Faculty with Emeritus Status      Back to Main

Faculty Detail    
Name RICHARD B MARCHASE
  
Campus Address THT 629 Zip 0006
Phone  (205) 934-9339
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 Emeritus

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.   
Su., Z., Csutora, P., Hunton, D., Shoemaker, R.L., Marchase, R.B., and Blalock, J.E. A Store-operated Non-selective Cation Channel in Lymphocytes is Activated Directly by Ca2+ Influx Factor (CIF) and Diacylglycerol. (2001) AJP: Cell 280(5): C1284-C1292.   
Trepakova, E.S., Csutora, P., Hunton, D.L., Marchase, R.B., Cohen, R.A., and Bolotina, V.M. Calcium influx factor (CIF) Directly Activates Store-Operated Cation Channels in Vascular Smooth Muscle Cells. (2000) J. Biol. Chem. 275:26158-26163.   
Holmes, E.W., et al. Measuring Contributions to the Research Mission of Medical Schools. (2000) Acad. Med. 75:304-313.   
Peng, J., Chen, P.Y., Marchase, R.B., and Prestwich, G.D. Preparation and Use of Photoactivatable Glucose-6-phosphate Analog. (2000) Bioorgan. Medic. Chem. Ltr. 10:535-539.   
Fu, L., Miseta, A., Hunton, D., Marchase, R.B., and Bedwell, D.M. Loss of the Major Isoform of Phosphoglucomutase Results in Altered Calcium Homeostasis in Saccharomyces cerevisiae. (2000) J. Biol. Chem. 275:5431-5440.   
 

Keywords
Ischemia, O-GlcNAC, Calcium