Publications

Scholarly Journals--Published

• Ahmed ASI, Sheng MHC, Lau KW, Wilson SM, Wongworawat MD, Tang X, Ghahramanpouri M, Nehme A, Xu Y, Abdipour A, Zhang XB, Wasnik S, Baylink DJ. Calcium released by osteoclastic resorption stimulates autocrine/paracrine activities in local osteogenic cells to promote coupled bone formation. Am J Physiol Cell Physiol. 2022 Apr 6. doi: 10.1152/ajpcell.00413.2021. PMID: 35385325. (04/2022) (link)
• Munoz K, Wasnik S, Abdipour A, Bi H, Wilson SM, Tang X, Ghahramanpouri M, Baylink DJ. The Effects of Insulin-Like Growth Factor I and BTP-2 on Acute Lung Injury. Int J Mol Sci. 2021 May 15;22(10):5244. doi: 10.3390/ijms22105244. PMID: 34063554 (05/2021) (link)
• Leslie E, Lopez V, Anti NAO, Alvarez R, Kafeero I, Welsh DG, Romero M, Kaushal S, Johnson CM, Bosviel R, Blaženovic I, Song R, Brito A, Frano MR, Zhang L, Newman JW, Fiehn O, Wilson SM. Gestational long-term hypoxia induces metabolomic reprogramming and phenotypic transformations in fetal sheep pulmonary arteries. Am J Physiol Lung Cell Mol Physiol. 2021 May 1;320(5):L770-L784. PMID: 33624555 (05/2021) (link)
• Hu XQ, Dasgupta C, Song R, Romero M, Wilson SM, Zhang L. MicroRNA-210 Mediates Hypoxia-Induced Repression of Spontaneous Transient Outward Currents in Sheep Uterine Arteries During Gestation. Hypertension. 2021 Apr;77(4):1412-1427. PMID: 33641365 (04/2021) (link)
• Song R, Hu XQ, Romero M, Holguin MA, Kagabo W, Xiao D, Wilson SM, Zhang L. Ryanodine receptor subtypes regulate Ca2+ sparks/spontaneous transient outward currents and myogenic tone of uterine arteries in pregnancy. Cardiovasc Res. 2021 Feb 22;117(3):792-804. PMID: 32251501 (02/2021) (link)
• Hu XQ, Song R, Romero M, Dasgupta C, Min J, Hatcher D, Xiao D, Blood A, Wilson SM, Zhang L. Gestational Hypoxia Inhibits Pregnancy-Induced Upregulation of Ca2+ Sparks and Spontaneous Transient Outward Currents in Uterine Arteries Via Heightened Endoplasmic Reticulum/Oxidative Stress. Hypertension. 2020 Sep;76(3):930-942. PMID: 32683903  (09/2020) (link)
• Wasnik S, Tang X, Bi H, Abdipour A, E Carreon E, Sutjiadi B, Lyu J, Zhang J, Wilson S, Baylink DJ. IGF-1 Deficiency Rescue and Intracellular Calcium Blockade Improves Survival and Corresponding Mechanisms in a Mouse Model of Acute Kidney Injury. Int J Mol Sci. 2020 Jun 8;21(11):4095. PMID: 32521790 (06/2020) (link)
• Song R, Hu XQ, Romero M, et al. Ryanodine Receptor Subtypes Regulate Ca2+ Sparks/STOCs and Myogenic Tone of Uterine Arteries in Pregnancy [published online ahead of print, 2020 Apr 6]. Cardiovasc Res. 2020;cvaa089. doi:10.1093/cvr/cvaa089 (04/2020) (link)
• Rood, K.; Lopez , V; La Frano, M.R; Fiehn, O;, Zhang, L; Blood, A.B.; Wilson, S.M. Gestational Hypoxia and Programing of Lung Metabolism. Front Physiol. 2019;10:1453. doi: 10.3389/fphys.2019.01453. Review. PMID: 31849704 (11/2019) (link)
• Moretta Dafne, Papamatheakis Demosthenes G., Morris Daniel P., Giri Paresh C., Blood Quintin, Murray Samuel, Ramzy Marian, Romero Monica, Vemulakonda Srilakshmi, Lauw Sidney, Longo Lawrence D., Zhang Lubo, Wilson Sean M. Long-Term High-Altitude Hypoxia and Alpha Adrenoceptor-Dependent Pulmonary Arterial Contractions in Fetal and Adult Sheep. Frontiers in Physiology. 10:2019.1032. DOI 10.3389/fphys.2019.01032 (08/2019) (link)
• Hu XQ, Song R, Romero M, Dasgupta C, Huang X, Holguin MA, Williams V, Xiao D, Wilson SM, Zhang L. Pregnancy Increases Ca2+ Sparks/Spontaneous Transient Outward Currents and Reduces Uterine Arterial Myogenic Tone. Hypertension. 2019 Mar;73(3):691-702. doi: 10.1161/HYPERTENSIONAHA.118.12484. PubMed PMID: 30661479; PubMed Central PMCID: PMC6374197.   (03/2019)
• Hashad AM, Harraz OF, Brett SE, Romero M, Kassmann M, Puglisi JL, Wilson SM, Gollasch M, Welsh DG. Caveolae Link CaV3.2 Channels to BKCa-Mediated Feedback in Vascular Smooth Muscle. Arterioscler Thromb Vasc Biol. 2018 Oct;38(10):2371-2381. doi: 10.1161/ATVBAHA.118.311394. PubMed PMID: 30354206. (10/2018)
• (07/2018)
• Ducsay CA, Goyal R, Pearce WJ, Wilson S, Hu XQ, Zhang L. Gestational Hypoxia and Developmental Plasticity. Physiol Rev. 2018 Jul 1;98(3):1241-1334. doi: 10.1152/physrev.00043.2017. Review. PubMed PMID: 29717932; PubMed Central PMCID: PMC6088145. (07/2018)
• Blum-Johnston C, Thorpe RB, Wee C, Opsahl R, Romero M, Murray S, Brunelle A, Blood Q, Wilson R, Blood AB, Zhang L, Longo LD, Pearce WJ, Wilson SM. Long-term hypoxia uncouples Ca2+ and eNOS in bradykinin-mediated pulmonary arterial relaxation. Am J Physiol Regul Integr Comp Physiol. 2018 Jun 1;314(6):R870-R882. doi: 10.1152/ajpregu.00311.2017. Epub 2018 Mar 7. PubMed PMID: 29513562; PubMed Central PMCID: PMC6032299. (06/2018)
• Liu T, Zhang M, Terry MH, Schroeder H, Wilson SM, Power GG, Li Q, Tipple TE, Borchardt D, Blood AB. Nitrite potentiates the vasodilatory signaling of S-nitrosothiols. Nitric Oxide. 2018 May 1;75:60-69. doi: 10.1016/j.niox.2018.01.011. Epub 2018 Feb 8. PubMed PMID: 29428841; PubMed Central PMCID: PMC5861029. (05/2018)
• Liu T, Zhang M, Terry MH, Schroeder H, Wilson SM, Power GG, Li Q, Tipple TE, Borchardt D, Blood AB. Hemodynamic Effects of Glutathione-Liganded Binuclear Dinitrosyl Iron Complex: Evidence for Nitroxyl Generation and Modulation by Plasma Albumin. Mol Pharmacol. 2018 May;93(5):427-437. doi: 10.1124/mol.117.110957. Epub 2018 Feb 23. PubMed PMID: 29476040; PubMed Central PMCID: PMC5878675. (05/2018)
• Hanson SFL, Terry MH, Moretta DT, Power GG, Wilson SM, Alam F, Ahsan F, Blood AB, Giri PC. Inhaled Fasudil Lacks Pulmonary Selectivity in Thromboxane-Induced Acute Pulmonary Hypertension in Newborn Lambs. J Cardiovasc Pharmacol Ther. 2018 Sep;23(5):472-480. doi: 10.1177/1074248418772814. Epub 2018 May 13. PubMed PMID: 29756460. (05/2018)
• Shen CP, Romero M, Brunelle A, Wolfe C, Dobyns A, Francis M, Taylor MS, Puglisi JL, Longo LD, Zhang L, Wilson CG, Wilson SM. Long-term high-altitude hypoxia influences pulmonary arterial L-type calcium channel-mediated Ca2+ signals and contraction in fetal and adult sheep. Am J Physiol Regul Integr Comp Physiol. 2018 Mar 1;314(3):R433-R446. doi: 10.1152/ajpregu.00154.2017. Epub 2017 Nov 22. PubMed PMID: 29167165; PubMed Central PMCID: PMC5899247. (03/2018)
• Hashad AM, Mazumdar N, Romero M, Nygren A, Bigdely-Shamloo K, Harraz OF, Puglisi JL, Vigmond EJ, Wilson SM, Welsh DG. Interplay among distinct Ca2+ conductances drives Ca2+ sparks/spontaneous transient outward currents in rat cerebral arteries. J Physiol. 2017 Feb 15;595(4):1111-1126. doi: 10.1113/JP273329. Epub 2016 Dec 12. PubMed PMID: 27805790; PubMed Central PMCID: PMC5309379. (02/2017)
• Hashad A M, Mazumdar N, Romero M, Nygren A, Bigdely-Shamloo K, . . . Welsh D G. (2017). Interplay among distinct Ca2+ conductances drives Ca2+ sparks/spontaneous transient outward currents in rat cerebral arteries. J Physiol, 595(4), 1111-1126. KEY POINTS: Distinct Ca2+ channels work in a coordinated manner to grade Ca2+ spark/spontaneous transient outward currents (STOCs) in rat cerebral arteries. The relative contribution of each Ca2+ channel to Ca2+ spark/STOC production depends upon their biophysical properties and the resting membrane potential of smooth muscle. Na+ /Ca2+ exchanger, but not TRP channels, can also facilitate STOC production. ABSTRACT: Ca2+ sparks are generated in a voltage-dependent manner to initiate spontaneous transient outward currents (STOCs), events that moderate arterial constriction. In this study, we defined the mechanisms by which membrane depolarization increases Ca2+ sparks and subsequent STOC production. Using perforated patch clamp electrophysiology and rat cerebral arterial myocytes, we monitored STOCs in the presence and absence of agents that modulate Ca2+ entry. Beginning with CaV 3.2 channel inhibition, Ni2+ was shown to decrease STOC frequency in cells held at hyperpolarized (-40 mV) but not depolarized (-20 mV) voltages. In contrast, nifedipine, a CaV 1.2 inhibitor, markedly suppressed STOC frequency at -20 mV but not -40 mV. These findings aligned with the voltage-dependent profiles of L- and T-type Ca2+ channels. Furthermore, computational and experimental observations illustrated that Ca2+ spark production is intimately tied to the activity of both conductances. Intriguingly, this study observed residual STOC production at depolarized voltages that was independent of CaV 1.2 and CaV 3.2. This residual component was insensitive to TRPV4 channel modulation and was abolished by Na+ /Ca2+ exchanger blockade. In summary, our work highlights that the voltage-dependent triggering of Ca2+ sparks/STOCs is not tied to a single conductance but rather reflects an interplay among multiple Ca2+ permeable pores with distinct electrophysiological properties. This integrated orchestration enables smooth muscle to grade Ca2+ spark/STOC production and thus precisely tune negative electrical feedback. (02/2017) (link)
• Liu T, Schroeder HJ, Zhang M, Wilson SM, Terry MH, Longo LD, Power GG, Blood AB. S-nitrosothiols dilate the mesenteric artery more potently than the femoral artery by a cGMP and L-type calcium channel-dependent mechanism. Nitric Oxide. 2016 Aug 31;58:20-7. doi: 10.1016/j.niox.2016.05.006. Epub 2016 May 25. PubMed PMID: 27235767; PubMed Central PMCID: PMC6322392. (08/2016)
• Liu T, Schroeder H J, Zhang M, Wilson S M, Terry M H, . . . Blood A B. (2016). S-nitrosothiols dilate the mesenteric artery more potently than the femoral artery by a cGMP and L-type calcium channel-dependent mechanism. Nitric Oxide, 58, 20-7. S-nitrosothiols (SNOs) are metabolites of NO with potent vasodilatory activity. Our previous studies in sheep indicated that intra-arterially infused SNOs dilate the mesenteric vasculature more than the femoral vasculature. We hypothesized that the mesenteric artery is more responsive to SNO-mediated vasodilation, and investigated various steps along the NO/cGMP pathway to determine the mechanism for this difference. In anesthetized adult sheep, we monitored the conductance of mesenteric and femoral arteries during infusion of S-nitroso-l-cysteine (L-cysNO), and found mesenteric vascular conductance increased (137 +/- 3%) significantly more than femoral conductance (26 +/- 25%). Similar results were found in wire myography studies of isolated sheep mesenteric and femoral arteries. Vasodilation by SNOs was attenuated in both vessel types by the presence of ODQ (sGC inhibitor), and both YC-1 (sGC agonist) and 8-Br-cGMP (cGMP analog) mediated more potent relaxation in mesenteric arteries than femoral arteries. The vasodilatory difference between mesenteric and femoral arteries was eliminated by antagonists of either protein kinase G or L-type Ca(2+) channels. Western immunoblots showed a larger L-type Ca(2+)/sGC abundance ratio in mesenteric arteries than in femoral arteries. Fetal sheep mesenteric arteries were more responsive to SNOs than adult mesenteric arteries, and had a greater L-Ca(2+)/sGC ratio (p = 0.047 and r = -0.906 for correlation between Emax and L-Ca(2+)/sGC). These results suggest that mesenteric arteries, especially those in fetus, are more responsive to SNO-mediated vasodilation than femoral arteries due to a greater role of the L-type calcium channel in the NO/cGMP pathway. (08/2016) (link)
• Giang M, Papamatheakis DG, Nguyen D, Paez R, Blum Johnston C, Kim J, Brunnell A, Blood Q, Goyal R, Longo LD, Wilson SM. Muscarinic Receptor Activation Affects Pulmonary Artery Contractility in Sheep: The Impact of Maturation and Chronic Hypoxia on Endothelium-Dependent and Endothelium-Independent Function. High Alt Med Biol. 2016 Jun;17(2):122-32. doi: 10.1089/ham.2015.0116. PubMed PMID: 27281473; PubMed Central PMCID: PMC4913491. (06/2016)
• Carla Blum-Johnston, Richard B Thorpe, Chelsea Wee, Monica Romero, Alexander R Brunelle, Quintin Blood, Rachael Wilson, Arlin B. Blood, Michael Francis, Mark S Taylor, Lawrence D. Longo, William J. Pearce, Sean M Wilson Developmental acceleration of bradykinin-dependent relaxation by prenatal chronic hypoxia impedes normal development after birth. American Journal of Physiology - Lung Cellular and Molecular Physiology Published 4 December 2015 Vol. no. , DOI: 10.1152/ajplung.00340.2015 (12/2015)
• Liu T, Schroeder HJ, Wilson SM, Terry MH, Romero M, Longo LD, Power GG, and Blood AB. Local and systemic vasodilatory effects of low molecular weight S-nitrosothiols. Free Radic Biol Med 91: 215-223, 2015.  (12/2015)
• Ardekani S, Scott H, Gupta S, Eum S, Yang X, Brunelle A, Wilson SM, Mohideen U, and Ghosh K. Nanoliposomal Nitroglycerin Exerts Potent Anti-Inflammatory Effects. Scientific Reports. Scientific Reports Nov 20;5:16258. doi: 10.1038/srep16258. (11/2015)
• Ardekani Soroush, Scott Harry A, Gupta Sharad, Eum Shane, Yang Xiao, . . . Ghosh Kaustabh. (2015). Nanoliposomal Nitroglycerin Exerts Potent Anti-Inflammatory Effects. Scientific Reports, 5, . Nitroglycerin (NTG) markedly enhances nitric oxide (NO) bioavailability. However, its ability to mimic the anti-inflammatory properties of NO remains unknown. Here, we examined whether NTG can suppress endothelial cell (EC) activation during inflammation and developed NTG nanoformulation to simultaneously amplify its anti-inflammatory effects and ameliorate adverse effects associated with high-dose NTG administration. Our findings reveal that NTG significantly inhibits human U937 cell adhesion to NO-deficient human microvascular ECs in vitro through an increase in endothelial NO and decrease in endothelial ICAM-1 clustering, as determined by NO analyzer, microfluorimetry, and immunofluorescence staining. Nanoliposomal NTG (NTG-NL) was formulated by encapsulating NTG within unilamellar lipid vesicles (DPhPC, POPC, Cholesterol, DHPE-Texas Red at molar ratio of 6: 2: 2: 0.2) that were similar to 155 nm in diameter and readily uptaken by ECs, as determined by dynamic light scattering and quantitative fluorescence microscopy, respectively. More importantly, NTG-NL produced a 70-fold increase in NTG therapeutic efficacy when compared with free NTG while preventing excessive mitochondrial superoxide production associated with high NTG doses. Thus, these findings, which are the first to reveal the superior therapeutic effects of an NTG nanoformulation, provide the rationale for their detailed investigation for potentially superior vascular normalization therapies. (11/2015) (link)
• Harraz O, Brett S, Zechariah A, Romero M, Puglisi J, Wilson S, Welsh D. Genetic ablation of CaV3.2 channels enhances the arterial myogenic response by modulating the RyR-BKCa axis. Arterioscler Thromb Vasc Biol 35: 1843-1851, 2015 (04/2015)
• Brunelle Alexander, Romero Monica, Puglisi Jose, Bers Donald, Izu Leighton, Longo Lawrence, & Wilson Sean. (2015). Effects of L-type Ca2+ Channel Facilitation on Ca2+ Spark Activity in Fetal Ovine Pulmonary Arterial Myocytes. FASEB Journal, 29, . (04/2015)
• Brunelle Alexander, Blum-Johnston Carla, Wee Chelsea, Blood Quintin, Wilson Rachael, . . . Wilson Sean. (2015). High altitude Gestation and Prenatal Programming of Bradykinin Induced Pulmonary Endothelial Ca2+ Responses and Arterial Vasorelaxation in Fetal and Newborn Lamb. FASEB Journal, 29, . (04/2015)
• Hutchinson TE, Zhong W, Chebolu S, Wilson SM, and Darmani N. L-type calcium channels contribute to 5-HT3-receptor-evoked CaMKIIa and ERK activation and induction of emesis in the least shrew (Cryptotis parva). European Journal of Physiology. 755:110-8. PMID25748600 (03/2015)
• Tao X, Lin MT, Thorington GU, Wilson SM, Longo LD, and Hessinger DA. Long-Term Hypoxia Increases Calcium Affinity of BK Channels in Ovine Fetal and Adult Cerebral Artery Smooth Muscle. American journal of physiology Heart and circulatory physiology. 2015; 308(7):H707-22. PMID25599571 (01/2015)
• Liu Taiming, Schroeder Hobe, Zhang Meijuan, Wilson Sean, Power Gordon, & Blood Arlin. (2014). Sheep mesenteric arteries are more sensitive to S-nitrosothiol-mediated vasodilation than femoral arteries due to an L-type calcium channel-dependent mechanism. Nitric Oxide-Biology and Chemistry, 42, 132-132. (11/2014) (link)
• Harraz Osama F, Abd El-Rahman Rasha R, Bigdely-Shamloo Kamran, Wilson Sean M, Brett Suzanne E, . . . Welsh Donald G. (2014). Ca(V)32 Channels and the Induction of Negative Feedback in Cerebral Arteries. Circ Res, 115(7), 650-U147. Rationale: T-type (Ca(V)3.1/Ca(V)3.2) Ca2+ channels are expressed in rat cerebral arterial smooth muscle. Although present, their functional significance remains uncertain with findings pointing to a variety of roles. Objective: This study tested whether Ca(V)3.2 channels mediate a negative feedback response by triggering Ca2+ sparks, discrete events that initiate arterial hyperpolarization by activating large-conductance Ca2+-activated K+ channels. Methods and Results: Micromolar Ni2+, an agent that selectively blocks Ca(V)3.2 but not Ca(V)1.2/Ca(V)3.1, was first shown to depolarize/constrict pressurized rat cerebral arteries; no effect was observed in Ca(V)3.2(-/-) arteries. Structural analysis using 3-dimensional tomography, immunolabeling, and a proximity ligation assay next revealed the existence of microdomains in cerebral arterial smooth muscle which comprised sarcoplasmic reticulum and caveolae. Within these discrete structures, Ca(V)3.2 and ryanodine receptor resided in close apposition to one another. Computational modeling revealed that Ca2+ influx through Ca(V)3.2 could repetitively activate ryanodine receptor, inducing discrete Ca2+-induced Ca2+ release events in a voltage-dependent manner. In keeping with theoretical observations, rapid Ca2+ imaging and perforated patch clamp electrophysiology demonstrated that Ni2+ suppressed Ca2+ sparks and consequently spontaneous transient outward K+ currents, large-conductance Ca2+-activated K+ channel mediated events. Additional functional work on pressurized arteries noted that paxilline, a large-conductance Ca2+-activated K+ channel inhibitor, elicited arterial constriction equivalent, and not additive, to Ni2+. Key experiments on human cerebral arteries indicate that Ca(V)3.2 is present and drives a comparable response to moderate constriction. Conclusions: These findings indicate for the first time that Ca(V)3.2 channels localize to discrete microdomains and drive ryanodine receptor-mediated Ca2+ sparks, enabling large-conductance Ca2+-activated K+ channel activation, hyperpolarization, and attenuation of cerebral arterial constriction. (09/2014) (link)
• Liu T, Schroeder HJ, Barcelo L, Bragg SL, Terry MH, Wilson SM, Power GG and Blood AB. Role of blood and vascular smooth muscle in the vasoactivity of nitrite. American journal of physiology Heart and circulatory physiology. 2014;307:H976-86. PMID25108012 (05/2014)
• Harraz Osama, Brett Suzanne, Wilson Sean, & Welsh Donald. (2014). Ca(V)32 knockout mice display enhanced myogenic tone due to reduced BKCa-mediated feedback. FASEB Journal, 28(1), . (04/2014)
• Glasgow Shane, Tao Xiaoxiao, Romero Monica, Osman Noah, Puglisi Jose, . . . Wilson Sean. (2014). Ontogeny, ryanodine receptor-mediated calcium sparks, and BK channel clustering in basilar arterial myocytes from long-term hypoxic sheep. FASEB Journal, 28(1), . (04/2014)
• Paez Ricardo, Romero Monica, Blood Quintin, Osman Noah, Manjunath Chetas, . . . Wilson Sean. (2014). cGMP amplification of pulmonary arterial myocyte Ca2+ waves is preferentially impaired in high altitude-induced hypoxic fetal sheep. FASEB Journal, 28(1), . (04/2014)
• Harraz OF, Abd El-Rahman RR, Bigdely-Shamloo K, Wilson SM, Brett SE, Romero M, Gonzales AL, Earley S, Vigmond EJ, Nygren A, Menon BK, Mufti RE, Watson T, Starreveld Y, Furstenhaupt T, Muellerleile PR, Kurjiaka DT, Kyle BD, Braun AP and Welsh DG. Ca(V)3.2 channels and the induction of negative feedback in cerebral arteries. Circulation research. 2014;115:650-61. PMID25085940 (01/2014)
• Yeo A, Liu T, Liu M, Noriega D, Wilson S M, & Blood A B. (2014). EFFECTS OF NITROSOTHIOLS ON METHACHOLINE-CONSTRICTED AIRWAY SMOOTH MUSCLE ISOLATED FROM ADULT RATS. Journal of Investigative Medicine, 62(1), 199-199. (01/2014)
• Giang M, Paez R, Kim J, Blood Q, Longo L, & Wilson S M. (2014). CHRONIC HYPOXIA SUPPRESSES MUSCARINIC INDUCED CONTRACTILITY IN INTACT OVINE PULMONARY ARTERIES. Journal of Investigative Medicine, 62(1), 178-179. (01/2014)
• Dobyns Abby, Shen Christine, Romero Monica, Wilson Chris, & Wilson Sean. (2014). Automated method for detecting correlated Ca2+ activity between multiple regions of interest. Journal of Vascular Research, 51, 141-141. (2014)
• Glasgow Shane, Tao Xiaoxiao, Romero Monica, Osman Noah, Puglisi Jose L, . . . Wilson Sean. (2014). Maturation, ryanodine receptor-mediated calcium sparks and BK channel clustering in basilar arterial myocytes from long term hypoxic sheep. Journal of Vascular Research, 51, 140-140. (2014)
• Harraz Osama, Hashad Ahmed, Zechariah Anil, Brett Suzanne, Wilson Sean, & Welsh Donald. (2014). Cav32 knockout mice display enhanced myogenic tone due to reduced BKCa-mediated feedback. Journal of Vascular Research, 51, 4-4. (2014)
• Harraz Osama, Abd-El Rahman Rasha, Bigdely Kamran, Wilson Sean, Brett Suzanne, . . . Welsh Donald. (2014). The induction of negative feedback in cerebral arteries by CaV32 channels. Journal of Vascular Research, 51, 139-139. (2014)
• Papamatheakis D G, Chundu M, Blood A B, & Wilson S M. (2013). Prenatal programming of pulmonary hypertension induced by chronic hypoxia or ductal ligation in sheep. Pulm Circ, 3(4), 757-80. Pulmonary hypertension of the newborn is caused by a spectrum of functional and structural abnormalities of the cardiopulmonary circuit. The existence of multiple etiologies and an incomplete understanding of the mechanisms of disease progression have hindered the development of effective therapies. Animal models offer a means of gaining a better understanding of the fundamental basis of the disease. To that effect, a number of experimental animal models are being used to generate pulmonary hypertension in the fetus and newborn. In this review, we compare the mechanisms associated with pulmonary hypertension caused by two such models: in utero ligation of the ductus arteriosus and chronic perinatal hypoxia in sheep fetuses and newborns. In this manner, we make direct comparisons between ductal ligation and chronic hypoxia with respect to the associated mechanisms of disease, since multiple studies have been performed with both models in a single species. We present evidence that the mechanisms associated with pulmonary hypertension are dependent on the type of stress to which the fetus is subjected. Such an analysis allows for a more thorough evaluation of the disease etiology, which can help focus clinical treatments. The final part of the review provides a clinical appraisal of current treatment strategies and lays the foundation for developing individualized therapies that depend on the causative factors. (12/2013) (link)
• Papamatheakis DG, Chundu M, Blood AB and Wilson SM. Prenatal programming of pulmonary hypertension induced by chronic hypoxia or ductal ligation in sheep. Pulmonary circulation. 2013;3:757-80. Invited Review (10/2013)
• (09/2013)
• Zhu R, X.Q. Hu, D. Xiao, S. Yang, S.M. Wilson, L.D. Longo, and L. Zhang. Chronic Hypoxia Inhibits Pregnancy-Induced Upregulation of SKCa Channel Expression and Function in Uterine Arteries. Hypertension, 62:367-74, 2013. PMID23716582 (09/2013)
• Papamatheakis D G, Blood A B, Kim J H, & Wilson S M. (2013). Antenatal Hypoxia and Pulmonary Vascular Function and Remodeling. Current Vascular Pharmacology, 11(5), 616-640. This review provides evidence that antenatal hypoxia, which represents a significant and worldwide problem, causes prenatal programming of the lung. A general overview of lung development is provided along with some background regarding transcriptional and signaling systems of the lung. The review illustrates that antenatal hypoxic stress can induce a continuum of responses depending on the species examined. Fetuses and newborns of certain species and specific human populations are well acclimated to antenatal hypoxia. However, antenatal hypoxia causes pulmonary vascular disease in fetuses and newborns of most mammalian species and humans. Disease can range from mild pulmonary hypertension, to severe vascular remodeling and dangerous elevations in pressure. The timing, length, and magnitude of the intrauterine hypoxic stress are important to disease development, however there is also a genetic-environmental relationship that is not yet completely understood. Determining the origins of pulmonary vascular remodeling and pulmonary hypertension and their associated effects is a challenging task, but is necessary in order to develop targeted therapies for pulmonary hypertension in the newborn due to antenatal hypoxia that can both treat the symptoms and curtail or reverse disease progression. (09/2013)
• Blood, A.B. M.H. Terry, J.M. Ross, G.G Power, L.D. Longo, and S.M. Wilson. Chronic perinatal hypoxia: pulmonary hypertension in newborn lambs by mechanisms independent of rho-kinase. American Journal of Physiology - Regulatory and Comparative Physiology, 304:R136-46, 2013 PMID23152110 (08/2013)
• Zhu R H, Hu X Q, Xiao D L, Yang S M, Wilson S M, Longo L D, & Zhang L B. (2013). Chronic Hypoxia Inhibits Pregnancy-Induced Upregulation of SKCa Channel Expression and Function in Uterine Arteries. Hypertension, 62(2), 367-374. Small-conductance Ca2+-activated K+ (SKCa) channels are crucial in regulating vascular tone and blood pressure. The present study tested the hypothesis that SKCa channels play an important role in uterine vascular adaptation in pregnancy, which is inhibited by chronic hypoxia during gestation. Uterine arteries were isolated from nonpregnant and near-term pregnant sheep maintained at sea level (approximate to 300 m) or exposed to high-altitude (3801 m) hypoxia for 110 days. Immunohistochemistry revealed the presence of SKCa channels type 2 (SK2) and type 3 (SK3) in both smooth muscles and endothelium of uterine arteries. The expression of SK2 and SK3 channels was significantly increased during pregnancy, which was inhibited by chronic hypoxia. In normoxic animals, both SKCa channel opener NS309 and a large-conductance (BKCa) channel opener NS1619 relaxed norepinephrine-contracted uterine arteries in pregnant but not nonpregnant sheep. These relaxations were inhibited by selective SKCa and BKCa channel blockers, respectively. NS309-induced relaxation was largely endothelium-independent. In high-altitude hypoxic animals, neither NS1691 nor NS309 produced significant relaxation of uterine arteries in either nonpregnant or pregnant sheep. Similarly, the role of SKCa channels in regulating the myogenic reactivity of uterine arteries in pregnant animals was abrogated by chronic hypoxia. Accordingly, the enhanced SKCa channel activity in uterine arterial myocytes of pregnant animals was ablated by chronic hypoxia. The findings suggest a novel mechanism of SKCa channels in regulating myogenic adaptation of uterine arteries in pregnancy and in the maladaptation of uteroplacental circulation caused by chronic hypoxia during gestation. (08/2013) (link)
• Papamatheakis D.G., A.B. Blood, J.H. Kim, and S.M. Wilson. Antenatal Hypoxia and Pulmonary Vascular Function and Remodeling. Current Vascular Pharmacology. 11:616-40, 2013 PMID24063380 Invited Review (01/2013)
• Blood A B, Terry M H, Merritt T A, Papamatheakis D G, Blood Q, . . . Wilson S M. (2013). Effect of chronic perinatal hypoxia on the role of rho-kinase in pulmonary artery contraction in newborn lambs. American Journal of Physiology-Regulatory Integrative and Comparative Physiology, 304(2), R136-R146. Blood AB, Terry MH, Merritt TA, Papamatheakis DG, Blood Q, Ross JM, Power GG, Longo LD, Wilson SM. Effect of chronic perinatal hypoxia on the role of rho-kinase in pulmonary artery contraction in newborn lambs. Am J Physiol Regul Integr Comp Physiol 304: R136-R146, 2013. First published November 14, 2012; doi:10.1152/ajpregu.00126.2012.-Exposure to chronic hypoxia during gestation predisposes infants to neonatal pulmonary hypertension, but the underlying mechanisms remain unclear. Here, we test the hypothesis that moderate continuous hypoxia during gestation causes changes in the rho-kinase pathway that persist in the newborn period, altering vessel tone and responsiveness. Lambs kept at 3,801 m above sea level during gestation and the first 2 wk of life were compared with those with gestation at low altitude. In vitro studies of isolated pulmonary arterial rings found a more forceful contraction in response to KCl and 5-HT in high-altitude compared with low-altitude lambs. There was no difference between the effects of blockers of various pathways of extracellular Ca2+ entry in low-and high-altitude arteries. In contrast, inhibition of rho-kinase resulted in significantly greater attenuation of 5-HT constriction in high-altitude compared with low-altitude arteries. High-altitude lambs had higher baseline pulmonary artery pressures and greater elevations in pulmonary artery pressure during 15 min of acute hypoxia compared with low-altitude lambs. Despite evidence for an increased role for rho-kinase in high-altitude arteries, in vivo studies found no significant difference between the effects of rho-kinase inhibition on hypoxic pulmonary vasoconstriction in intact high-altitude and low-altitude lambs. We conclude that chronic hypoxia in utero results in increased vasopressor response to both acute hypoxia and serotonin, but that rho-kinase is involved only in the increased response to serotonin. (01/2013) (link)
• Hadley S R, Blood Q, Rubalcava M, Waskel E, Lumbard B, . . . Wilson S M. (2012). Maternal high-altitude hypoxia and suppression of ryanodine receptor-mediated Ca2+ sparks in fetal sheep pulmonary arterial myocytes. American Journal of Physiology-Lung Cellular and Molecular Physiology, 303(9), L799-L813. Hadley SR, Blood Q, Rubalcava M, Waskel E, Lumbard B, Le P, Longo LD, Buchholz JN, Wilson SM. Maternal high-altitude hypoxia and suppression of ryanodine receptor-mediated Ca2+ sparks in fetal sheep pulmonary arterial myocytes. Am J Physiol Lung Cell Mol Physiol 303: L799-L813, 2012. First published August 31, 2012; doi:10.1152/ajplung.00009.2012.-Ca2+ sparks are fundamental Ca2+ signaling events arising from ryanodine receptor (RyR) activation, events that relate to contractile and dilatory events in the pulmonary vasculature. Recent studies demonstrate that long-term hypoxia (LTH) can affect pulmonary arterial reactivity in fetal, newborn, and adult animals. Because RyRs are important to pulmonary vascular reactivity and reactivity changes with ontogeny and LTH we tested the hypothesis that RyR-generated Ca2+ signals are more active before birth and that LTH suppresses these responses. We examined these hypotheses by performing confocal imaging of myocytes in living arteries and by performing wire myography studies. Pulmonary arteries (PA) were isolated from fetal, newborn, or adult sheep that lived at low altitude or from those that were acclimatized to 3,801 m for > 100 days. Confocal imaging demonstrated preservation of the distance between the sarcoplasmic reticulum, nucleus, and plasma membrane in PA myocytes. Maturation increased global Ca2+ waves and Ca2+ spark activity, with sparks becoming larger, wider, and slower. LTH preferentially depressed Ca2+ spark activity in immature pulmonary arterial myocytes, and these sparks were smaller, wider, and slower. LTH also suppressed caffeine-elicited contraction in fetal PA but augmented contraction in the newborn and adult. The influence of both ontogeny and LTH on RyR-dependent cell excitability shed new light on the therapeutic potential of these channels for the treatment of pulmonary vascular disease in newborns as well as adults. (11/2012) (link)
• Hu X Q, Xiao D L, Zhu R H, Huang X H, Yang S M, Wilson S M, & Zhang L B. (2012). Chronic Hypoxia Suppresses Pregnancy-Induced Upregulation of Large-Conductance Ca2+-Activated K+ Channel Activity in Uterine Arteries. Hypertension, 60(1), 214-222. Our previous study demonstrated that increased Ca2+-activated K+ (BKCa) channel activity played a key role in the normal adaptation of reduced myogenic tone of uterine arteries in pregnancy. The present study tested the hypothesis that chronic hypoxia during gestation inhibits pregnancy-induced upregulation of BKCa channel function in uterine arteries. Resistance-sized uterine arteries were isolated from nonpregnant and near-term pregnant sheep maintained at sea level (approximate to 300 m) or exposed to high-altitude (3801 m) hypoxia for 110 days. Hypoxia during gestation significantly inhibited pregnancy-induced upregulation of BKCa channel activity and suppressed BKCa channel current density in pregnant uterine arteries. This was mediated by a selective downregulation of BKCa channel beta 1 subunit in the uterine arteries. In accordance, hypoxia abrogated the role of the BKCa channel in regulating pressure-induced myogenic tone of uterine arteries that was significantly elevated in pregnant animals acclimatized to chronic hypoxia. In addition, hypoxia abolished the steroid hormone-mediated increase in the beta 1 subunit and BKCa channel current density observed in nonpregnant uterine arteries. Although the activation of protein kinase C inhibited BKCa channel current density in pregnant uterine arteries of normoxic sheep, this effect was ablated in the hypoxic animals. The results demonstrate that selectively targeting BKCa channel beta 1 subunit plays a critical role in the maladaption of uteroplacental circulation caused by chronic hypoxia, which contributes to the increased incidence of preeclampsia and fetal intrauterine growth restriction associated with gestational hypoxia. (Hypertension. 2012; 60:214-222.) (07/2012) (link)
• Hadley, H.R., Q. Blood, M. Rubalcava, E. Waskel, B. Lumbard, P. Le, L.D. Longo, J.N. Buchholz and S.M. Wilson. Maternal high altitude hypoxia and suppression of ryanodine receptor mediated Ca2+ sparks in pulmonary arterial myocytes of fetal sheep. Am J Physiol – Lung Cell and Mol Physiol. 303:L799-813, 2012 PMID22962012 (06/2012)
• Hu, X-Q, D. Xiao, R. Zhu, X. Huang, S. Yang, S.M. Wilson and L. Zhang. Chronic Hypoxia Suppresses Pregnancy-Induced Upregulation of Large-Conductance Ca2+-Activated K+ Channel Activity in Uterine Arteries. Hypertension. 60: 214-222, 2012PMID22665123 (05/2012)
• Papamatheakis, D.G, J.J. Patel , Q. Blood, T.T. Merritt, L.D. Longo, and S.M. Wilson. Depolarization-dependent contraction increase after birth and preservation following long-term hypoxia in sheep pulmonary arteries. Pulmonary Circulation, 2:41-53, 2012. PMID22558519 (01/2012)
• Hu X Q, Xiao D, Zhu R, Huang X, Yang S, Wilson S, & Zhang L. (2011). Pregnancy upregulates large-conductance Ca2+-activated k+ channel activity and attenuates myogenic tone in uterine arteries. Hypertension, 58(6), 1132-9. Uterine vascular tone significantly decreases whereas uterine blood flow dramatically increases during pregnancy. However, the complete molecular mechanisms remain elusive. We hypothesized that increased Ca(2+)-activated K(+) (BK(Ca)) channel activity contributes to the decreased myogenic tone of uterine arteries in pregnancy. Resistance-sized uterine arteries were isolated from nonpregnant and near-term pregnant sheep. Electrophysiological studies revealed a greater whole-cell K(+) current density in pregnant compared with nonpregnant uterine arteries. Tetraethylammonium and iberiotoxin inhibited K(+) currents to the same extent in uterine arterial myocytes. The BK(Ca) channel current density was significantly increased in pregnant uterine arteries. In accordance, tetraethylammonium significantly increased pressure-induced myogenic tone in pregnant uterine arteries and abolished the difference in myogenic responses between pregnant and nonpregnant uterine arteries. Activation of protein kinase C produced a similar effect to tetraethylammonium by inhibiting BK(Ca) channel activity and increasing myogenic tone in pregnant uterine arteries. Chronic treatment of nonpregnant uterine arteries with physiologically relevant concentrations of 17beta-estradiol and progesterone caused a significant increase in the BK(Ca) channel current density. Western blot analyses demonstrated a significant increase of the beta1, but not alpha, subunit of BK(Ca) channels in pregnant uterine arteries. In accordance, steroid treatment of nonpregnant uterine arteries resulted in an upregulation of the beta1, but not alpha, subunit expression. The results indicate that the steroid hormone-mediated upregulation of the beta1 subunit and BK(Ca) channel activity may play a key role in attenuating myogenic tone of the uterine artery in pregnancy. (12/2011) (link)
• Goyal R., D.G. Papamatheakis, M. Loftin, K. Vrancken, A.S. Dawson, N.J. Osman, A.B. Blood, W.J. Pearce, L.D. Longo, and S.M. Wilson. Long-term maternal hypoxia: the role of extracellular Ca2+ entry during serotonin-mediated contractility in fetal ovine pulmonary arteries. Reproductive sciences 18: 948-962, 2011. PMID21960509 (05/2011)
• Hu X.Q., D. Xiao, R. Zhu, X. Huang, S. Yang, S. Wilson S and L. Zhang. Pregnancy upregulates large-conductance Ca(2+)-activated K(+) channel activity and attenuates myogenic tone in uterine arteries. Hypertension 58, 1132-1139, 2011. PMID3223357 (03/2011)
• Blood A.B., H.J. Schroeder, M.H. Terry, J. Merrill-Henry, S.L. Bragg, K. Vrancken, T. Liu, J.L. Herring, L.C. Sowers, S.M. Wilson, and G.G. Power. Inhaled nitrite reverses hemolysis-induced pulmonary vasoconstriction in newborn lambs without blood participation. Circulation 123: 605-612, 2011. PMID3077283 (01/2011)
• Hume, J.R., C.E. McAllister, S.M. Wilson. Inhibition of InsP3 responses and capacitative calcium entry by caffeine in canine pulmonary arterial smooth muscle cells. Vascular Pharmacology. 50:89-97, 2009.   (03/2009)
•  Goyal, R., J.E. Angermann, O. Ostrovskaya, G.D. Smith, S.M. Wilson. Intracellular Ca2+ homeostasis is modified with aging in murine mesenteric arterial smooth muscle cells. Experimental Gerontology. 44:201-207, 2009.   (02/2009)
•  Behringer, E.J, C.K. Vanterpool, W.J. Pearce, W.J., S.M. Wilson, J.N. Buchholz. Advancing age alters the contribution of calcium release from smooth endoplasmic reticulum stores in superior cervical ganglion cells. Journal of Gerontology, 64: 34-44. 2009.   (02/2009)
•  Goyal, R., K.D. Creel, E. Chavis, G.D. Smith, L.D. Longo, S.M. Wilson. Maturation of intracellular calcium homeostasis in sheep pulmonary arterial smooth muscle cells. American Journal of Physiology – Lung Cellular Molecular Physiology. 295:L905 - L914, 2008.   (12/2008)
• Ostrovskaya, O., R. Goyal, C.E. McAllister, I.N. Pessah, J.R. Hume, S.M. Wilson. FLA 365 as an inhibitor of ryanodine receptor signaling in canine pulmonary arterial myocytes. Journal of Pharmacology and Experimental Therapeutics. 323:381-90, 2007.   (10/2007)
•  Ng, L.C., S.M. Wilson, C.E. McAllister, and J.R. Hume. Roles of InsP3 and ryanodine receptors in capacitative Ca2+ entry in canine pulmonary arterial smooth muscle cells. British Journal of Pharmacology [shared co-authorship with L.C. Ng]. 152:101-11, 2007.   (06/2007)
• C. del Corsso, O. Ostrovskaya, C E McAllister, K Murray, W J Hatton, A M Gurney, N J Spencer, S M Wilson. Effects of aging on Ca2+ signaling in murine mesenteric arterial smooth muscle cells. Mechanisms of Aging and Development, 127:315-323, 2006.   (06/2006)
•  Ng, L.C., S.M. Wilson and J.R. Hume. Mobilization of SR Stores by Hypoxia Leads to Consequent Activation of Capacitative Ca2+ Entry in Isolated Canine Pulmonary Arterial Smooth Muscle Cells. Journal of Physiology.563: 409-419, 2005.   (06/2005)
•  Wilson S.M., H.S. Mason, L.C. Ng, S. Montague, L. Johnston, N. Nicholson, S. Mansfield, and J.R. Hume.  Role of extracellular Ca2+ entry during 5-HT induced vasoconstriction of canine pulmonary arteries. British Journal of Pharmacology. 144: 252-264, 2005.   (06/2005)
• Hermoso, M.,  C.M. Satterwhite, Y Andrade, J Hidalgo, S.M. Wilson, B. Horowitz, and J.R. Hume.  ClC-3 is a fundamental molecular component of volume-sensitive outwardly rectifying Cl- channels and volume regulation in HeLa Cells and Xenopus laevis oocytes.  Journal of Biological Chemistry, 277:40066, 2002.    (06/2002)
•  Wilson, S.M., H.S. Mason, G.D. Smith, L. Johnston, N. Nicholson, R. Janiak, and J.R. Hume.  Comparative capacitative calcium entry mechanisms in canine pulmonary and renal arterial smooth muscle cells.  Journal of Physiology, 543:917-931, 2002.   (06/2002)
• Janiak,R.,S.M. Wilson, S. Montague, and J.R. Hume. Characteristics of intracellular Ca2+ stores and elementary release events in canine pulmonary arterial smooth muscle cells.  American Journal of Physiology Cell Physiology. 280:C22-33, 2001.    (06/2001)
• Wilson, S.M., S.C. Lee, S. Shook, and P.A. Pappone. Purinergic and b-adrenergic stimulation enhance inactivation of a voltage-gated potassium current.  American Journal of Physiology Cell Physiology. 279:C1847-1858, 2000.    (06/2000)
• Wilson S.M., M.J. Barsoum, B.W. Wilson, and P.A. Pappone. Purine nucleotides modulate proliferation of brown fat preadipocytes. Cell Proliferation. 32:131-140, 1999.    (06/1999)
• Wilson S.M., Pappone P.A. P2 receptor modulation of voltage-gated potassium currents in brown adipocytes. Journal of General Physiology. 113:125-138, 1999.    (06/1999)

Abstract

• Yoo T, Romero M, Puglisi J, Bers D M, Izu L, Longo L D, & Wilson S M. (2015). THE EFFECT OF ACUTE HYPOXIA ON RYR ACTIVITY IN HIGH ALTITUDE ACCLIMATIZED FETAL AND ADULT SHEEP. Journal of Investigative Medicine, 63(1), 99-99. (01/2015)
• Kaushal Shawn, Romero Monica, Osman Noah, Paez Ricardo, Francis Michael, . . . Wilson Sean. (2014). Oxidative stress and the impact of prenatal chronic hypoxia on ryanodine receptor generated calcium responses in fetal pulmonary arterial myocytes. FASEB Journal, 28(1), . (04/2014)
• Wee C L, Blum-Johnston C, Blood Q, Wilson R H, Blood A B, Longo L D, & Wilson S M. (2013). Underdeveloped bradykinin-dependent vasorelaxation in immature pulmonary arteries from long term hypoxic sheep is not due to loss of cGMP signaling. FASEB Journal, 27, 1. (04/2013)
• Paez R, Rubalcava M, Blood Q, Hong S, Francis M, . . . Wilson S M. (2013). Postnatal-related changes in cAMP mediated pulmonary arterial relaxation and calcium signals persist following long term hypoxia in sheep. FASEB Journal, 27, 1. (04/2013)
• Blum-Johnston C, Blood Q, Wee C, Wilson R, Blood A B, Longo L D, & Wilson S. (2013). Bradykinin-induced pulmonary vasorelaxation is modified by long term hypoxia and postnatal maturation in sheep. FASEB Journal, 27, 1. (04/2013)
• Abd El-Rahman R, Harraz O, Bigdely-Shamloo K, Mufti R, Gonzales A, . . . Welsh D. (2013). Ca(V)32 Channels and the Induction of Negative Feedback in Cerebral Arterial Smooth Muscle. FASEB Journal, 27, 1. (04/2013)
• Davitt E, Liu T, Wilson S, & Blood A. (2013). SENSITIVITY OF THE MESENTERIC ARTERY OF FETAL AND ADULT SHEEP TO NITRIC OXIDE AND LOW MOLECULAR WEIGHT NITROSOTHIOLS. Journal of Investigative Medicine, 61(1), 190-190. (01/2013)
• Rubalcava M, Osman N J, Blood Q, Kim J H, Longo L D, & Wilson S M. (2012). Cyclic Nucleotides Cause Divergent Ryanodine Receptor Modulation in Pulmonary Arterial Myocytes from Immature Chronic Hypoxic Sheep. Faseb Journal, 26, . (04/2012)
• Paez R, Nguyen D, Papamatheakis D, Kim J, Blood Q, Longo L D, & Wilson S M. (2012). Maternal Hypoxemia Suppresses Muscarinic Acetylcholine Receptor Dependent Contraction of Pulmonary Arteries from Fetal Sheep. Faseb Journal, 26, . (04/2012)
• Kim J, Blood Q, Longo L D, & Wilson S M. (2012). mAChR Dependent Contraction of Pulmonary Arteries with Functional Endothelium from Chronically Hypoxic Fetal and Adult Sheep. Faseb Journal, 26, . (04/2012)
• Lumbard B, Waskel E, Paez R, Blood Q, Rubalcava M, . . . Wilson S M. (2012). Myoendothelial Junction Formation is Restricted in Pulmonary Arteries of Fetal Sheep. Faseb Journal, 26, . (04/2012)
• Kim J H, Longo L D, & Wilson S M. (2012). ATTENUATED BETA ADRENERGIC RECEPTOR MEDIATED PULMONARY VASODILATION IN HIGH ALTITUDE TERM-FETAL SHEEP. Journal of Investigative Medicine, 60(1), 216-216. (01/2012)
• Donovan V, Coats J, Badaut J, Wilson S, Huang L, & Obenaus A. (2011). LONG-TERM WHITE MATTER CHANGES IN A BILATERAL MODEL OF REPETITIVE MILD TRAUMATIC BRAIN INJURY. Journal of Neurotrauma, 28(6), A81-A81. (06/2011)
• Donovan V, Coats J, Badaut J, Wilson S, Huang L, & Obenaus A. (2011). LONG-TERM WHITE MATTER CHANGES IN A BILATERAL MODEL OF REPETITIVE MILD TRAUMATIC BRAIN INJURY. Journal of Neurotrauma, 28(6), A81-A81. (06/2011)
• Papamatheakis D, Vemulakonda S, Patel J, Blood Q, Merritt T, Longo L D, & Wilson S M. (2011). POSTNATAL MATURATION DECREASES THE ROLE OF RHO-KINASE IN ELECTROMECHANICAL COUPLING OF SHEEP PULMONARY ARTERIES. Journal of Investigative Medicine, 59(1), 133-134. (01/2011)
• Hadley S R, Blood Q, Le P, Longo L D, Buchholz J, . . . Wilson S M. (2011). ONTOGENY AND HIGH ALTITUDE INFLUENCE CA(2+) SPARKS IN SHEEP PULMONARY ARTERIAL MYOCYTES. Journal of Investigative Medicine, 59(1), 131-131. (01/2011)
• Hunt D I, Chang M, Blood Q K, Merrit T A, Wilson S M, & Blood A B. (2010). THE VASODILATORY EFFECTS OF SURFACTANT ON LUNG AND SYSTEMIC ARTERIES. Journal of Investigative Medicine, 58(1), 108-108. (01/2010)
• Hunt D I, Chang M, Blood Q K, Merrit T A, Wilson S M, & Blood A B. (2010). THE VASODILATORY EFFECTS OF SURFACTANT ON LUNG AND SYSTEMIC ARTERIES. Journal of Investigative Medicine, 58(1), 138-138. (01/2010)
• Papamatheakis D, Blood Q, Merritt T, Lauw S, & Wilson S. (2010). MATURATION AND CHRONIC HYPOXIA INFLUENCE ALPHA ADRENERGIC FUNCTION IN THE PULMONARY VASCULTURE OF SHEEP. Journal of Investigative Medicine, 58(1), 138-138. (01/2010)
• Vemulakonda S, Papamatheakis D G, Forrest A, Leblanc N, Angermann J, Longo L D, & Wilson S M. (2010). CALCIUM ACTIVATED CHLORIDE CHANNELS IN PULMONARY ARTERIAL VASOCONSTRICTION ARE INFLUENCED BY POSTNATAL MATURITY AND LONG-TERM HYPOXIC STRESS. Journal of Investigative Medicine, 58(1), 137-137. (01/2010)
• Blood A B, Vrancken K, Schroeder H, Wilson S M, Terry M H, Merrill-Henry J, & Power G G. (2009). PRODUCTION OF NITRIC OXIDE FROM NITRITE IN THE LUNG. Journal of Physiological Sciences, 59, 263-263. (2009)

Books and Chapters

• Wilson, S.M.  and N. Leblanc. Chapter 1. Membrane Electrical Properties of Vascular Smooth Muscle Cells of the Pulmonary Circulation. In Ion Channels in the Pulmonary Vasculature. Edited by X.J. Yuan. Marcel Dekker Publisher. ISBN: 0-8247-5968-0. 2005   (06/2005)