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Faculty Detail     Name JOHN C CHATHAM   Campus Address VH G038 Zip 0019 Phone 205-934-0240 E-mail jchatham@uab.edu Other websites

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Pathology   Molecular & Cellular Pathology Professor Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Center  Center for Aging  Center for Aging Professor Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor Center  Medicine  Comprehensive Diabetes Ctr Professor Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Professor Center  General Clinical Research Center  Ctr for Free Radical Bio Professor Center  Medicine  Ctr Cardiovasc Bio Professor

Graduate Biomedical Sciences Affiliations Cell, Molecular, & Developmental Biology  Cellular and Molecular Biology Program  Integrative Biomedical Sciences  Medical Scientist Training Program  Molecular and Cellular Pathology Program  Pathobiology and Molecular Medicine

Biographical Sketch  John Charles Chatham was born in Didmarton, Gloucestershire, England in May 1960. He received a B.Sc. (Hons) degree in Chemistry from the University of Southampton England (1983) and a D.Phil. in Biochemistry from University of Oxford (1987). In 1987 he moved to the USA first to a postdoctoral fellowship at Huntington Medical Research Institutes, Pasadena, CA and then to Department of Radiology at Johns Hopkins University School of Medicine. After his postdoctoral training he joined the faculty at Johns Hopkins School of Medicine first as an Instructor and then as an Assistant Professor in the Department of Radiology. He earned the title of Associate Professor of Medicine after coming to UAB in 2000.

Society Memberships Organization Name Position Held Org Link American Diabetes Association      American Heart Association      American Physiology Society      International Society for Heart Research

Research/Clinical Interest Title Cardiomyocyte function and metabolism in diabetes and ischemic heart disease Description The overall goal of his laboratory is to understand the impact of alterations in cardiac energy metabolism and substrate utilization on the cardiomyocyte function. We have three major areas of interest: 1) Investigating the mechanisms leading to the increased incidence of heart failure in patients with diabetes and 2) development of new metabolically based therapeutic interventions for the treatment of ischemic heart disease 3) development of metabolic interventions to improve outcomes following trauma and hemorrhage. A common theme to all these projects is the role glucose in post-translational modifications of proteins mediated by the hexosamine biosynthesis pathway leading to protein-O-glycosylation. We propose that this is a central mechanism by which changes in metabolism are transduced into alterations in cellular function. Projects currently underway in our laboratory includes studies involving isolated cardiomyocytes, intact isolated perfused hearts and whole animal models. We use 13C and 1H nuclear magnetic resonance (NMR) spectroscopy to determine metabolic fluxes in the intact heart. In addition, we also use a range of standard physiological, biochemical and molecular techniques. We are also currently exploring proteomic and mass spectrometric methods for the identification and characterization of O-glycosylated proteins.

Selected Publications  Publication PUBMEDID Zou L, Yang S, Hu S, Chaudry IH, Marchase RB, Chatham JC. The protective effects of PUGNAc on cardiac function after trauma-hemorrhage are mediated via increased protein O-GlcNAc levels.  17414423  Marsh SA, Powell PC, Agarwal A, Dell'italia LJ, Chatham JC. Cardiovascular dysfunction in Zucker obese and Zucker diabetic fatty rats: the role of hydronephrosis. Am J Physiol Heart Circ Physiol. 2007 Mar 9; [Epub ahead of print]   17351065   Fulop N, Zhang Z, Marchase RB, Chatham JC Glucosamine cardioprotection in perfused rat hearts associated with increased O-linked N-acetylglucosamine protein modification and altered p38 activation. Am J Physiol Heart Circ Physiol. 2007 May;292(5):H2227-36.  17208994   Wang P, Fraser H, Lloyd SG, McVeigh JJ, Belardinelli L, Chatham JC. A comparison between ranolazine and CVT-4325, a novel inhibitor of fatty acid oxidation, on cardiac metabolism and left ventricular function in rat isolated perfused heart during ischemia and reperfusion. J Pharmacol Exp Ther. 2007 Apr;321(1):213-20.  17202401  Fulop N, Mason MM, Dutta K, Wang P, Davidoff AJ, Marchase RB, Chatham JC. Impact of Type 2 diabetes and aging on cardiomyocyte function and O-linked N-acetylglucosamine levels in the heart. Am J Physiol Cell Physiol. 2007 Apr;292(4):C1370-8.   17135297  Liu J, Marchase RB, Chatham JC Glutamine-induced protection of isolated rat heart from ischemia/reperfusion injury is mediated via the hexosamine biosynthesis pathway and increased protein O-GlcNAc levels. J Mol Cell Cardiol. 2007 Jan;42(1):177-85   17069847  Liu J, Marchase RB, Chatham JC. Glutamine-induced protection of isolated rat heart from ischemia/reperfusion injury is mediated via the hexosamine biosynthesis pathway and increased protein O-GlcNAc levels. J Mol Cell Cardiol. 2007 Jan;42(1):177-85.   17069847   Fulop N, Marchase RB, Chatham JC. Role of protein O-linked N-acetyl-glucosamine in mediating cell function and survival in the cardiovascular system. Cardiovasc Res. 2007 Jan 15;73(2):288-97.   16970929   Champattanachai V, Marchase RB, Chatham JC. Glucosamine protects neonatal cardiomyocytes from ischemia-reperfusion injury via increased protein-associated O-GlcNAc. Am J Physiol Cell Physiol. 2007 Jan;292(1):C178-87.   16899550  Yang S, Zou, L-Y, Bounelis P, Chaudry I, Chatham JC and Marchase RB. Glucosamine administration during resuscitation improves organ function following trauma-hemorrhage. Shock 25: 600-607, 2006.  16721268  First Prev   1 2 3 4 of  4  Next Last

Keywords Myocardial ischemia, diabetic cardiomyopathy, hypovolemic shock

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