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Faculty Detail     Name RICHARD B MARCHASE   Campus Address AB 720E Zip 0107 Phone 205-934-1294 E-mail marchase@uab.edu Other websites http://www.uab.edu/research

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Secondary  Neurobiology  Neurobiology Professor Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor Center  Pathology   Cell Adhesion & Matrix Research Center Professor Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor Center  Medicine  Comprehensive Diabetes Ctr Professor Center  General Clinical Research Center  Comprehensive Neuroscience Center Professor Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor Center  General Clinical Research Center  Minority Health & Research Center Professor

Graduate Biomedical Sciences Affiliations Neuroscience Graduate Program  Neurosciences

Biographical Sketch  Richard B. Marchase, Ph.D. is the UAB Vice President for Research and the Senior Associate Dean for Research in the School of Medicine. His administrative functions include strategic planning, regulatory oversight, recruitment, and space allocation for a research enterprise generating approximately $450 million annually. Marchase received his undergraduate degree with honors in 1970 from Cornell University, and was honored with the Hamilton Award as the Outstanding Graduate in Science and Engineering. He received his Ph.D. from The Johns Hopkins University in 1976 and did postdoctoral training at Duke University. He was named a member of the faculty there in 1978 and was honored as a Nanaline H. Duke Scholar. In 1984 he received one of the inaugural Presidential Young Investigator Awards from the National Science Foundation. Dr. Marchase was recruited to the University of Alabama at Birmingham in the Department of Cell Biology in 1986 as an Associate Professor. He was promoted to Professor in 1990 and was named Chair in 1994. He became Associate Dean in 2000 and Vice President in 2004. Dr. Marchase maintains an active research laboratory supported by the National Institutes of Health. He is a past Associate Editor of The Anatomical Record and was on the editorial board of the American Journal of Physiology:Cell. He is currently on the Editorial Board of the journal SHOCK. He was presented with the Mary Jane Kugle Award from the Juvenile Diabetes Research Foundation in 1999. Marchase is active in several national organizations. He served as President of the Association of Anatomy, Cell Biology, and Neurobiology Chairs and as a member of the National Caucus of Basic Biomedical Science Chairs. He serves on the steering committee of the American Association of Medical Colleges’ Group on Research Advancement and Development. He is currently Vice President of the Federation of American Societies for Experimental Biology, which represents 23 professional organizations and is recognized as the principal voice of the biomedical research community on issues related to research funding and research integrity.

Society Memberships Organization Name Position Held Org Link American Association for the Advancement of Science      American Association of Anatomists   Former Associate Editor    American Physiological Society   Editorial Board    Association of Anatomy, Cell Biology, and Neurobiology Chairpersons   Past President    Federation of American Societies for Experimental Biology   Vice President    SHOCK Society   Editorial Board

Research/Clinical Interest Title Calcium, Capacitative Calcium Entry, Hexosamine Biosynthesis Pathway, Trauma Hemorrhage, O-linked Cytoplasmic Glycosylation Description Novel cell and organ protection therapies that decrease tissue damage during and following stresses such as ischemia would have profound clinical implications. Our data demonstrate that in a rat model of hypovolemic stress, the infusion of lactated Ringer's solution containing glucosamine leads to a striking improvement in post-trauma function. We also have demonstrated that glucosamine is highly protective in isolated heart models of ischemia/reperfusion and calcium overload. We propose that this protection results from an amplification of a naturally occurring, stress-activated, pro-survival pathway that is characterized by increased flux through the hexosamine biosynthesis pathway (HBP) and leads to increased levels of the nucleotide sugar UDP-N-acetylglucosamine (UDP-GlcNAc), the substrate for a glycosylation reaction that is now well-characterized but highly atypical. It is our hypothesis that an elevation in the levels of protein-associated O-GlcNAc is a critical adaptive response that increases the chances of survival of both the organism and the cell during and following periods of stress. In addition, we hypothesize that interventions that amplify and/or accelerate the increases in O-GlcNAc greatly decrease the cellular and tissue damage that would otherwise result from a stress, in particular hypovolemic stress and ischemia. As a corollary, we claim that one means of achieving this protection occurs because an increase in O-GlcNAc inhibits the calcium overload that can result from stress and often leads to cell death.

Selected Publications  Publication PUBMEDID Liu1, J., Pang1 Y., Chang, T. Wang, P., Bounelis, P., Chatham, J. and Marchase, R.B. Ischemic Injury Protection Transduced by Hyperglycemia and Hexosamine Biosynthesis. Submitted.    Kneass, Z. and Marchase, R.B. Protein O-GlcNAc modulates motility-associated signaling intermediates in neutrophils. (2005) J. Biol. Chem. 280(15):14579-14585.    Kneass, Z., and Marchase, R.B. Neutrophils Exhibit Rapid Agonist-Induced Increases in Protein-Associated O-GlcNAc. (2004) J. Biol. Chem. J. Biol. Chem. 279(44):45759-45765.    Su, Z., Shoemaker, R.L., Marchase, R.B., and Blalock, J.E. Ca2+ modulation of Ca2+ release activated-Ca2+ is Responsible for the Inactivation of its Monovalent Cation Current. (2004) Biophys. J. 86:805-814.    Pang, Y., Chatham, J.C., and Marchase, R.B. The Hexosamine Pathway Is Responsible for the Inhibition by Diabetes of Phenylephrine-Induced Inotropy. (2004) Diabetes. 53:1074-1081    Hunton, D.L., Zou, L.Y., Pang, Y., and Marchase, R.B. Adult Rat Cardiomyocytes Exhibit Capacitative Calcium Entry. (2004) Am. J. Physiol. 286:H1124-H1132.    Su, Z., Barker, D.S., Csutora, P., Chang, T., Shoemaker, R.L., Marchase, R.B., and Blalock, J.E. Regulation of Ca2+ Release Activated Ca2+ Channels by INAD and Calcium Influx Factor. (2002) AJP:Cell. 284(2): C497-C505.    Pang, Y. and Marchase, R.B. Hyperglycemia Inhibits Capacitative Calcium Entry and Hypertrophy in Neonatal Cardiomyocytes. (2002) Diabetes. 51:3461-3467.    Tsukamoto, H., Tousson, A., Circolo, A., Marchase, R.B., and Volanakis, J.E. Calnexin is Associated with and Induced by Overexpressed Human Complement Protein. (2002) The Anat. Rec. 267:7-16.    Hunton, D.L., Lucchesi, P.A., Pang, Y., Dell’Italia, L.J., and Marchase, R.B. Capacitative Calcium Entry Contributes to NFAT Nuclear Translocation and Hypertrophy in Cardiomyocytes. (2002) J. Biol. Chem. 277:14266-14273.    First Prev   1 2 of  2  Next Last

Keywords Ischemia, O-GlcNAC, Calcium

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