Gregory L. Brower, DVM, Ph.D.
Centenary Associate Professor
TEXAS A&M UNIVERSITY
B.S. Veterinary Science
Awarded - December 1985
TEXAS A&M UNIVERSITY, College of Veterinary Medicine
Doctor of Veterinary Medicine
Awarded - May 1987
UNIVERSITY OF MISSOURI-COLUMBIA
Residency - Laboratory Animal Pathology
June 1992 - December 1993
Ph .D. Biomedical Sciences
Awarded - December 1998
Dr. Brower's major research emphasis is focused on understanding the pathogenesis of heart failure. Specifically, the mechanisms and regulatory events influencing cardiac remodeling induced by chronic ventricular volume or pressure overload. Ventricular enlargement, consisting of both hypertrophy and dilatation, together with a thin walled, spherical ventricular shape are known risk factors associated with congestive heart failure. Preventing this adverse myocardial remodeling is a major goal of this laboratory. Ongoing research currently includes determining:
- the role of cardiac mast cells, cytokines (i.e., TNF-alpha), and adhesion proteins (i.e., integrins) in myocardial remodeling and in maintaining normal ventricular shape, size, and function.
- the role of myocardial matrix metalloproteinases (MMPs) in extracellular matrix synthesis and degradation.
- the temporal response at the cellular and organ level in cardiac myocyte remodeling responsible for hypertrophy and dilatation.
- the role of angiotensin II mediated myocardial hypertrophy and damage in the pathogenesis of heart failure.
- the mechanisms responsible for the gender related differences in myocardial remodeling and the cardioprotective effects of female sex hormones and or phytoestrogens.
These research objectives involve the use of animal models of hypertension (e.g., ascending aortic banding and angiotensin II infusions) and chronic ventricular volume overload (e.g., arteriovenous fistula and myocardial infarction); and several disciplines including organ and isolated myocyte physiology, biochemistry, pathology, immunohistochemistry, morphometry, pharmacology, and molecular biology. Much of this research is performed in the Cardiac Structure and Function Laboratory in collaboration with Dr. Joseph Janicki and Dr. Jason Gardner.
- Brower GL, Henegar JR and Janicki JS. Temporal evaluation of left ventricular remodeling and function in rats with chronic volume overload. American Journal of Physiology Heart and Circulatory Physiology 271 (5 Pt 2): H2071-H2078, 1996.
- Brower GL and Janicki JS. Contribution of ventricular remodeling to pathogenesis of heart failure in rats. American Journal of Physiology Heart and Circulatory Physiology 280(2): H674-H683, 2001.
- de Almeida A, Mustin D, Forman MF, Brower GL, Janicki JS and Carver W. Effects of mast cells on the behavior of isolated heart fibroblasts: Modulation of collagen remodeling and gene expression.Journal of Cellular Physiology 191(1): 51-59, 2002.
- Chancey AL, Brower GL, Peterson JT and Janicki JS. Effects of matrix metalloproteinase inhibition on ventricular remodeling due to volume overload. Circulation 105(16): 1983-1988, 2002.
- Gardner JD, Brower GL and Janicki JS. Gender differences in cardiac remodeling secondary to chronic volume overload. Journal of Cardiac Failure 8(2): 101-107, 2002.
- Chancey AL, Brower GL and Janicki JS. Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function.American Journal of Physiology Heart and Circulatory Physiology282(6): H2152-H2158, 2002.
- Brower GL, Chancey AL, Thanigaraj S, Matsubara BB and Janicki JS. Cause and effect relationship between myocardial mast cell number and matrix metalloproteinase activity. American Journal of Physiology Heart and Circulatory Physiology 283(2): H518-H525, 2002.
- Stewart, JA, Jr, Wei CC, Brower GL, Rynders PE, Hankes GH, Dillon AR, Lucchesi PA, Janicki JS and Dell'Italia LJ. Cardiac mast cell- and chymase-mediated matrix metalloproteinase activity and left ventricular remodeling in mitral regurgitation in the dog. Journal of Molecular and Cellular Cardiology 35(3): 311-319, 2003.
- Brower GL, Gardner JD and Janicki JS. Protection from adverse cardiac remodeling induced by chronic volume overload is abolished by ovariectomy. Molecular and Cellular Biochemistry 251:89-95, 2003.
- Janicki JS, Brower GL, Gardner JD, Chancey AL, and Stewart, JA, Jr. The dynamic interaction between matrix metalloproteinase activity and adverse myocardial remodeling. Heart Failure Reviews 9(1): 33-42, 2004.
- Forman MF, Brower GL and Janicki JS. Spontaneous histamine secretion during isolation of rat cardiac mast cells. Inflammation Research 53: 453-457, 2004.
- Murray DB, Gardner JD, Brower GL and Janicki JS. Endothelin-1 mediates cardiac mast cell degranulation, matrix metalloproteinase activation and myocardial remodeling in rats. American Journal of Physiology Heart and Circulatory Physiology 287(5): H2295-H2299, 2004.
- Brower GL and Janicki JS. Pharmacologic inhibition of mast cell degranulation prevents left ventricular remodeling induced by chronic volume overload in rats. Journal of Cardiac Failure 11(7): 548-556, 2005.
- Chancey AL, Gardner JD, Murray DB, Brower GL and Janicki JS. Modulation of cardiac mast mediated extracellular matrix degradation by estrogen. American Journal of Physiology Heart and Circulatory Physiology 289(1): H316-H321, 2005.
- Gardner JD, Brower GL and Janicki JS. Effect of dietary phytoestrogens on cardiac remodeling secondary to chronic volume overload in female rats. Journal of Applied Physiology 99(4): 1378-1383, 2005.
- Janicki JS, Brower GL, Gardner JD, Forman MF, Stewart Jr JA, Murray DB, and Chancey AL. Regulation of myocardial matrix metalloproteinases in mediating the ventricular remodeling response to sustained volume or pressure overload. Cardiovascular Research69(3): 657-665, 2006.
- Forman MF, Brower GL and Janicki JS. Rat cardiac mast cell maturation and differentiation following acute ventricular volume overload. Inflammation Research In Press, 2006.
- Brower GL , Gardner JD, Forman MF, Murray DB, Voloshenyuk T, Levick SP and Janicki JS. The relationship between myocardial extracellular matrix remodeling and ventricular function. European Journal of Cardio-Thoracic Surgery In Press, 2006.