Biography

Dr. Liu started his postdoctoral training at the University of Connecticut Health Center (UHC) in 2006. Before that he had been a Neurologist in Wannan Medical College Yijishan Hospital (China) for seven years. After 5-year postdoc training Dr. Liu was promoted to Assistant Professor of Neuroscience at UHC in 2012. Dr. Liu joined the Department of Neurology at the University of Texas McGovern Medical School in 2015 and serves as the Director of Translational Stroke Research in addition to his commitment to teaching. His research is currently supported by NIH funding.

Education

Masters Degree
Neuroscience, Wannan Medical College, Wuhu, China
Medical Degree
Bengbu Medical College, Bengbu, China
Residency
Neurology, Yijishan Hospital, Anhui, China

Areas of Interests

Research Interests

Ischemic stroke

Research Information

Research interests in Dr. Liu’s lab focus on innate immune responses to cerebral ischemia. Microglial activation is a key element in initiating and perpetuating inflammatory responses to stroke. Microglial responses are characterized as either M1, classical activation (pro-inflammatory), or M2, alternative activation (anti-inflammatory). The two distinct phenotypes of microglia potentially provide a therapeutic avenue that selectively enhances M2 and/or inhibits M1 activation. We hypothesize that interferon regulatory factor 5 (IRF5) and IRF4 function through TLR4-MyD88-IRF5 and IL4R-Jmjd3-IRF4 pathways to regulate microglial M1/M2 phenotype respectively, and that manipulation of the IRF5-IRF4 regulatory axis confers neuroprotection against ischemia. Another research direction in this lab studies the sexual dimorphism in hypoxic-ischemic encephalopathy (HIE) that is a major cause of neonatal death and long-term disability. The mechanisms underlying the “male sensitive” phenotype of HIE are unknown; we are employing both genetic and pharmacologic techniques to explore the pathways that mediate the sexual dimorphism in HIE. These exploratory studies will lead to better understanding of sex-specific mechanisms in HIE and will help us identify and optimize biological targets for therapeutic intervention in children.