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Jorge A. Bezerra, MDProfessor; Director, Digestive Health CenterWilliam and Rebecca Balistreri Chair of Pediatric Hepatology Department of Pediatrics; Division of Gastroenterology, Hepatology and NutritionVisit the Bezerra Lab Site
Dr. Bezerra investigates regulatory mechanisms of liver and biliary injury. One major research focus is pre-clinical and translational research on biliary atresia, the most common cause of chronic liver disease in children. He has used large-scale expression arrays and bioinformatics to develop transcriptional maps for human and murine biliary atresia. These maps generated hypotheses regarding pathogenic mechanisms of disease. Testing these hypotheses in the laboratory, he is dissecting the cellular and molecular basis of neonatal injury and obstruction of extrahepatic bile ducts using unique in vitro and experimental models of disease. Studies have identified key regulatory functions for hepatic dendritic cells and CD8+ and NK lymphocytes in recognition and induction of cell death in the bile duct epithelium. Ongoing experiments are identifying co-stimulatory signals controlling cell survival during early postnatal development and small molecules regulating biliary diseases. In translational studies, he is also applying state-of-the-art approaches to identify the molecular determinants of treatment response in multi-center studies of children with biliary atresia and syndromes of intrahepatic cholestasis.
Dr. Bezerra has used the Bioinformatics, Microarray, and Integrative Morphology Cores in collaboration with Drs. Chougnet, Aronow, Miethke, Shivakunmar and Tiao in patient- and animal-based experiments to interrogate the pathogenic mechanisms of biliary atresia. He also collaborates with Drs. Mattner and Ridgway studying mechanisms of biliary injury in models of primary biliary cirrhosis. Projection of Core use: Gene and Protein Expression, Bioinformatics, and Integrative Morphology Cores.
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Immunofluorescence panels (left) identify population of portal tracts by NK cells (CD56) and T cells (CD3) in livers with molecular signature of inflammation. Photos on right depict the same tissue sections depicted on the left after nuclear staining with DAPI (white bar = 50 μm). Graphs on right show average number of stained cells in portal tracts. *P < 0.05.Figurefrom Genome Med, 2010;2:33.
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