Phu Tran is an Associate Professor in the Department of Pediatrics. His research focuses on mechanisms (molecular and epigenetic) underlying the long-term effects of early-life adversity on neural development. His lab has been investigating how early-life (fetal and early postnatal) environmental exposures (nutritional deficiency, opioids) result in long-term neural gene dysregulation associated with altered epigenetic signatures. His lab employs cutting-edge technology (ATACseq/ChIPseq/Single-cell sequencing/exosomes) to probe these changes in cord blood stem cells and rodent hippocampal cells with an ultimate goal to establish non-invasive biomarkers for brain development and health. His other research interests include molecular mechanisms regulating post-operative pain, neonatal hypoxic-ischemic brain injury, and nicotinic acetylcholine receptor chaperones.
Our research activities focus on two major goals. First, we investigate the long-term effects of early-life iron deficiency on hippocampal function. Iron deficiency is a major global health concern that affects conservatively 2 billion individuals worldwide, including about 30% of pregnant women and pre-school age children.It is well established that early-life iron deficiency has long lasting negative effects on cognition and socio-emotional behaviors in humans despite prompt iron treatment following diagnosis.These long-term effects constitute a significant cost to society in terms of educational attainment, job potential, and mental health.Thus, understanding at the cellular and molecular level how early iron deficiency affects brain development in animal models may lead to important insights into alternative therapeutic development to prevent and treat at risk pregnancies and children with iron deficiency. Second, we investigate the biological role of TMEM35A (NACHO) in the nervous system. TMEM35A has been shown to function as a chaperone for neuronal nicotinic acetylcholine receptors, which have been implicated in neuropathologies and psychopathologies (e.g., addiction, pain, Autism, Alzheimer, and schizophrenia). Defining the precise molecular function of this novel chaperone using a gene knockout mouse model and drug treatment is promising in defining new mechanisms and pathways that regulate cognition, pain, and addictive behaviors.The work may lead to new strategies to improving quality of life and productivity.