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Weibiao Cao received MD from Zhejiang Medical University, Hangzhou, China in 1986. From 1986 to 1995 he worked as a resident, chief resident and attending physician in the Department of Medicine, Peking Union Medical College Hospital, Beijing China. In 1995 he was hired as a Postdoctoral research assistant at the University of Calgary, Canada. In February, 1996, Dr. Cao joined Gsatrointestinal Motility Research Lab, Department of Medicine, Rhode Island Hospital and The Warren Alpert Medical School of Brown University. He was promoted as an assistant professor in Brown University in 2001. Dr. Cao has received two R21 grants and one R01 grant from NIH.
Dr. Weibiao Cao studies the signal transduction pathways mediating contraction in normal esophageal smooth muscle and the inflammation-associated changes in signaling that occur in experimental esophagitis. His findings show that a low molecular weight phospholipase A2 (type I) mediates cat and human in vitro lower esophageal sphincter tone by producing arachidonic acid, which is metabolized to prostaglandin F2alpha and thromboxane A2. These arachidonic acid metabolites act on receptors linked to Gi3 and Gq proteins to activate phospholipases, producing second messengers, and maintaining LES tone. He also investigates inflammation-induced changes in contractile signal transduction pathways of human sigmoid colon and study the effect of inflammatory mediators on colonic motor function in ulcerative colitis. His findings demonstrate that hydrogen peroxide and IL-1beta may play an important role in motor dysfunction in ulcerative colitis. Currently he is studying the mechanisms of the progression from Barrett esophagus to esophageal adenocarcinoma, focusing on the role of NADPH oxidases-derived reactive oxygen species. His research on NADPH oxidase NOX5-S shows that NADPH oxidase NOX5-S is overexpressed in esophageal adenocarcinoma cells and mediates acid-induced hydrogen peroxide production. Acid-induced NOX5-S expression depends on an increase in intracellular calcium and activation of a transcription factor CREB. NOX5-S contributes to increased cell proliferation and decreased apoptosis in esophageal adenocarcinoma cells.
|Editorial: J Gastrointest Dig Syst 2012, 2: e108|
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