Research Projects

Microglia, brain macrophages, play a crucial role in protecting the brain from pathogens and maintaining brain homeostasis. They secrete growth factors and clear tissue debris through phagocytosis, which is essential for neurodevelopment. Altered microglial activity is linked to altered neurobehavior and neuroinflammatory diseases. Microglial phagocytosis is regulated by specific receptors, regulatory molecules, and signaling pathways. PU.1, a transcription factor known for microglial proliferation, may also be involved in microglial phagocytosis. However, the exact molecular mechanism of PU.1 mediated regulation of microglial phagocytosis is yet to be revealed. TREM2, a phagocytic receptor associated with myelin, amyloid beta, dead cell debri clearance, and synaptic pruning, plays a vital role in EAE pathogenesis. Arsenic exposure increases microglial phagocytosis in vitro and in ex vivo microglia isolated from arsenic and cuprizone-treated animals. The hypothesis is that arsenic exposure increases microglial phagocytosis through TREM2 by controlling PU.1 expression. The study aims to study the effect of arsenic on PU.1 expression, find the underlying mechanism of arsenic-induced altered expression of PU.1, and check the impact of altered microglial phagocytosis in a cuprizone-induced demyelinating mouse model.