Roy McCauley, Ph.D.
Roy McCauley, Ph.D.
540 E. Canfield, 6275 Scott Hall
Detroit, Michigan 48201
Office Phone(313) 577-6737
Office Fax(313) 577-6739
Ischemia is the reduction of arterial blood flow to a tissue. In heart muscle, this leads to oxygen and glucose deprivation and failure of the mitochondria to produce cellular energy. Upon restoration of blood flow (that is, reperfusion), the myocytes become reoxygenated, and various free radicals of oxygen are formed. These free radicals cause to cellular damage which, in turn, can lead to cell death by either apoptosis or necrosis. Our research on ischemia/reperfusion injury is part of a long collaboration with Dr. Tiziano Scarabelli, also a member of the Pharmacology Department.
Some of our most interesting work involves urocortin, a 40 amino acid peptide that is related to the corticotrophin releasing factor (CRF) family. Urocortin is endogenously synthesized by several organs, including the heart. Importantly, its synthesis and release are increased during cardiac ischemia, where urocortin acts to protect myocytes against injury upon binding to its cognate receptors on the surface of cardiac cells. We recently documented that cardiac urocortin is released in the blood stream of rats exposed to ischemia/reperfusion injury before the occurrence of myocyte necrosis and apoptosis. Therefore, the quantification of urocortin serum levels may be clinically useful in the diagnosis of heart attacks.
More recently, we have investigated the role that macro-autophagy has in ischemia. When mouse atrial cells were exposed to ischemic conditions, autophagy proceeded at normal rates even though cellular ATP fell to as low as 15% of normal. That these cells would budget scant amounts of ATP to support autophagy suggests that it is important for surviving the ischemic event, This hypothesis was supported by the observations that supplementation of hypoxic cells with glucose increased ATP, autophagy and cell survival while inhibition of autophagy with 7-methyl adenosine decreased survival.
BS in microbiology (1965) and PhD in pharmacology (1970) from the Ohio State University
Post doctoral research an Cornell University (1970-1972)
Sabbatical research at Biozentrum, Basel CH (1988-1989)
Sabbatical research at Monash University, Melbourne, Australia
NJH postdoctoral fellowship (1970-1972)
Fogarty fellowship (1988-1989)
Areas of Expertise
- Latchman D, Saravolatz L, Faggian G, Mazzucco M, Chowdrey H, Stephanou A, Scarabelli TM. Cardiac release of urocortin precedes the occurrence of irreversible myocardial damage in the rat heart exposed to ischemia/reperfusion injury. FEBS Letter. 2008 Mar 19;582(6):984-90.
- Chen Scarabelli C, McCauley RB, Yuan Y, Di Rezze J, Patel D, Putt J, Raddino R, Allebban Z, Abboud J, Scarabelli GM, Chilukuri K, Gardin J, Saravolatz L, Faggian G, Mazzucco A, Scarabelli TM. Oral administration of amino acidic supplements improves protein and energy profiles in skeletal muscle of aged rats: elongation of functional performance and acceleration of mitochondrial recovery in adenosine triphosphate after exhaustive exertion. Am J Cardiol. (2008) 101 (11A) 42E-48E.
- Scarabelli TM, Townsend PA, Chen Scarabelli C, Yuan Z, McCauley RB, Di Rezze J, Patel D, Putt J, Allebban Z, Abboud J, Chilukuri K, Gardin J, Saravolatz L, Knight RA, Latchman DS, Stephanou A. Amino acid supplementation differentially modulates STAT1 and STAT3 activation in the myocardium exposed to ischemia/reperfusion injury. Am J Cardiol. (2008) 101 (11A) 63E-68E.
- E. Kuizon, E.G. Pearce, C. Chen-Scarabelli, Z. Yuan, K. Abounit, R.B. McCauley, L. Saravolatz, G. Faggain, P.A. Townsend and T.M. Scarabelli. Mechanisms of action and clinical implications of cardiac urocortin: a journey from the heart to the systemic circulation, with a stopover in the mitochondria. Int. J. Cardiol. (2009) 137 189-194.
- Abounit, K., Scarabelli, T. and McCauley, R., Autophagy in mammalian cells World Journal of Biological Chemistry 2012 Jan. 26 3(1) 1-6