Overview In this proposal, we will test our hypothesis that mutant ECs cause bAVM formation and progression through stimulating excessive angiogenesis, impairing pericyte function and induction of inflammation. We will show that mutant ECs undergo clonal expansion and release angiogenic factors to stimulate the proliferation of adjacent normal endothelial cells. We will also show that mutant EC impair pericyte function through reduction of PDGFB mediated ANG1, TGFb1 and PDGFRb expression in pericytes and that mutant EC drives microglia activation, macrophage, and lymphocyte infiltration through induction of EC-inflammation. The overarching goal of this project is to identify new therapeutic targets. Affiliated Lab Center for Cerebrovascular Research Principal investigator UCSF Hua Su, MD Professor in Residence Collaborators UCSF Judith Hellman, MD Professor, Vice Chair of Research External persons Tom Arnold, MD Associate Professor in Residence Pediatrics Akiko Hata, PhD Professor, Cardiovascular Research Institute Support this research Are you excited by the innovative work we’re doing on this project? Learn how your financial support can make the difference in our work. Support
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