Shannon S. Glaser, PhD

Education and Training

• Texas A&M University System Health Science Center, PhD, 2006
• Texas A&M University, MS, 1994
• Texas A&M University, BS, 1991

Research Interests

• Proliferation of cholangiocytes is critical for the maintenance of biliary mass and secretory function during the pathogenesis of chronic cholestatic liver diseases, such as primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC). We have previously demonstrated that proliferating cholangiocytes serve as a neuroendocrine compartment during liver disease pathogenesis and as such secrete and respond to hormones and neuropeptides contributing to the autocrine and paracrine pathways that modulate liver inflammation and fibrosis. We have recently obtained novel data indicating that cholangiocytes express a local renin-angiotensin-system (RAS) and that chronic administration of angiotensin II (Ang II) increases the proliferation of normal rat cholangiocytes and enhances the proliferation of cholangiocytes during extrahepatic cholestasis induced by bile duct ligation (BDL). We have also obtained unique in vitro preliminary data demonstrating that mechanical stress, which occurs during extrahepatic obstructive disorders, induces cholangiocyte proliferation via mechanical activation of the angiotensin type 1 receptor (AT1). AT1 is known to regulate proliferation as a G-protein coupled receptor binding Ang II and as a mechanoreceptor that can induce proliferation in response to mechanical stress in the absence of Ang II in other cell types. However, the contribution of the RAS to the pathogenesis of cholangiocytes during cholestatic liver diseases remains to be established. The long-range natural progression of my research program will be to determine how activation of the local RAS mechanical stress and other factors contribute to biliary fibrosis during cholestatic liver diseases.