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Joseph S. Janicki, Ph.D.


Title:

Professor and Chairman

PUBMED Link:

Janicki JS

Research:

Dr. Janicki's research is focused on two aspects of cardiac remodeling secondary to abnormal pressure or volume loading conditions. The first deals with the role of the tissue renin-angiotensin system, including tissue angiotensin converting enzyme activity, in the cardiomyocyte hypertrophic response. The second involves the regulation of myocardial collagenase activity and the role that activated collagenase plays in progressive left ventricular dilatation. Ventricular enlargement, together with wall thinning and sphericalization, are features of chronic myocardial failure that contribute to its relentless downhill course. Preventing this adverse architectural and geometrical remodeling process is a major goal of this laboratory. These two research objectives are related in that hypertrophy is a major risk factor for heart failure. This research involves the use of animal models of hypertension, ventricular volume overload and heart failure, and several disciplines including organ and isolated myocyte physiology, biochemistry, pharmacology, morphometry and molecular biology.

Research Lab


Recent Publications:

  • Brower GL, Gardner JD and Janicki JS. Gender mediated cardiac protection from adverse ventricular remodeling is abolished by ovariectomy. Mol Cell Biochem, 251:89-95, 2003.
  • 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. J Mol Cell Cardiol J Mol Cell Cardiol 35:311-319, 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 Fail Reviews 9: 33-42, 2004.
  • Murray DB, Gardner JD, Brower GL, Janicki JS: Endothelin-1 mediates cardiac mast cell degranulation, matrix metalloproteinase activation and myocardial remodeling in rats. Am J Physiol. 287:H2295-H2299, 2004.
  • Janicki JS, Brower GL, Chancey AL, Forman MF and Jobe LJ. Cardiac mast cells as mediators of ventricular remodeling. In Interstitial Fibrosis in Heart Failure. F Villareal (ed), Springer Science & Business Media, Inc., New York, 2004, pp197-209.
  • Forman MF, Brower GL and Janicki JS. Spontaneous histamine secretion during isolation of rat cardiac mast cells. Inflam Res 53: 453-457, 2004.
  • Brower GL and Janicki JS. Pharmacologic inhibition of mast cell degranulation prevents left ventricular remodeling induced by chronic volume overload in rats. J Card Fail 11: 548-556, 2005.
  • Chancey AL, Gardner JD, Murray DB, Brower GL and Janicki JS. Modulation of cardiac mast mediated extracellular matrix degradation by estrogen. Am J Physiol 289: 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. J Applied Physiol 99: 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 Research (In Press)

Education:

Ph.D. Physiology & Biophysics, University of Alabama, Birmingham, Alabama
M.S.E. Fluid Mechanics, Catholic University, Washington, D.C.
B.S. Physics, University of Delaware, Newark, Delaware.

Contact Information:

Phone: (803) 733-3233
Fax: (803) 733-1533
jjanicki@gw.med.sc.edu
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