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Dr. Yan Zhang, Research Assistant Professor

Department of Biological Sciences, Michigan Technological University

Abstract: 

Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic disorder (frequency 1:400-1:1,000) affecting more than 600,000 Americans and 12.5 million people worldwide. ADPKD is caused by mutations in PKD1 or PKD2 which encode polycystin-1 (PC-1) and polycystin-2 (PC-2), respectively. The disease is characterized by the continuous formation and growth of numerous fluid-filled cysts in the kidneys. Aberrant innate immune responses play pivotal roles in driving cyst growth and disease progression in ADPKD; however, the precise molecular mechanisms remain poorly understood. Our recent experiments using human ADPKD cells and mouse models showed that activation of toll-like receptor 2 (TLR2) in cystic epithelial cells stimulated ERK-mediated proliferation and NF-κB-mediated expression of inflammatory cytokines and chemokines. Our study provides insight into the molecular mechanisms by which innate immunity promotes disease progression and suggests that TLR2 is a therapeutic target for ADPKD treatment.