About Qing Yi Ma, PhD

Research Focus

Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of neonatal mortality and long-term neurological disabilities. Despite extensive research on neuronal injury, the role of the developing cerebrovascular system in HIE pathogenesis remains poorly understood.

Our laboratory investigates the mechanisms of cerebrovascular dysfunction, blood-brain barrier injury, and neuroinflammation in neonatal brain injury, with a particular focus on the critical role of brain pericytes in neurovascular development and disease. We seek to understand how developmental-stage-specific responses of the neurovascular unit influence both acute injury and long-term neurodevelopmental outcomes following hypoxic-ischemic insult.

Current Research Areas

1. Brain Pericytes, Blood-Brain Barrier maturation and Dysfunction in Neonatal HIE

Brain pericytes are essential for postnatal blood-brain barrier maturation, and vascular stability and integrity. Using newly developed pericyte-specific reporter mice, conditional gene knockout models, and primary cell culture systems, we investigate the molecular mechanisms underlying pericyte vulnerability during neonatal HIE. Our current studies focus on the TBK1 signaling pathway and its role in regulating pericyte survival, neurovascular integrity, and inflammatory responses following injury.

2. Neurovascular Remodeling and Long-Term Developmental Outcomes

Neonatal HIE often results in lifelong neurological deficits. Beyond acute injury, we study how hypoxic-ischemic insults alter postnatal cerebrovascular development, leading to vascular regression, maladaptive remodeling, and impaired neurovascular maturation. By identifying the cellular and molecular mechanisms affecting both pericytes and endothelial cells, we aim to uncover therapeutic strategies that promote healthy vascular development and improve long-term outcomes.

3. Prenatal Hypoxia and Fetal Brain Vulnerability

Susceptibility to neonatal brain injury is often established before birth. We investigate how prenatal hypoxia reprograms the fetal neurovascular system and increases vulnerability to subsequent HIE. A major focus is the hypoxia-responsive microRNA, miR-210, known as the "master hypoxamir." We hypothesize that miR-210 drives pericytes toward an immature, remodeling phenotype characterized by metabolic reprogramming and enhanced vulnerability to injury.

Long-Term Goal

Our ultimate goal is to define the developmental neurovascular mechanisms that govern susceptibility and recovery after neonatal brain injury and to identify novel therapeutic targets that protect the developing brain from hypoxic-ischemic and ischemic insults.

Research Approach

Our laboratory employs multidisciplinary approaches that integrate: Transgenic mouse models with cell-specific reporters and gene deletion, Seahorse metabolic profiling, Confocal and imaging, Flow cytometry, Primary neurovascular cell culture systems, Experimental models of neonatal and prenatal hypoxic-ischemic injury, and ischemic stroke model.