Newsletter
References:
- Baskin K, Taegtmeyer H. Taking Pressure Off the Heart: The Ins and Outs of Atrophic Remodeling. Cardiovasc Res. 2011 Feb 25.
- Khalaf KI, Taegtmeyer H. Insulin sensitizers and heart failure: an engine flooded with fuel. Curr Hypertens Rep. 2010 Dec;12(6):399-401. No abstract available.
- Taegtmeyer H, Stanley WC. Too much or not enough of a good thing? Cardiac glucolipotoxicity versus lipoprotection. J Mol Cell Cardiol. 2011 Jan;50(1):2-5. Epub 2010 Sep 24. No abstract available.
- Ballal K, Wilson CR, Harmancey R, Taegtmeyer H. Obesogenic high fat western diet induces oxidative stress and apoptosis in rat heart. Mol Cell Biochem. 2010 Nov;344 (1-2):221-30.
- Algahim MF, Lux TR, Leichman JG, Boyer AF, Miller CC 3rd, Laing ST, Wilson EB, Scarborough T, Yu S, Snyder B, Wolin-Riklin C, Kyle UG, Taegtmeyer H. Progressive regression of left ventricular hypertrophy two years after bariatric surgery. Am J Med. 2010 Jun;123(6):549-55. Erratum in: Am J Med. 2010 Oct;123(10):e13.
- Taegtmeyer H. Tracing cardiac metabolism in vivo: one substrate at a time. J Nucl Med. 2010 May 1;51 Suppl 1:80S-87S. Review.
- Taegtmeyer H, Sen S, Vela D. Return to the fetal gene program: a suggested metabolic link to gene expression in the heart. Ann N Y Acad Sci. 2010 Feb;1188:191-8. Review
- Razeghi, P., Baskin, K.K., Sharma, S., Young, M.E., Stepkowski, S., Essop, M., Taegtmeyer, H. (2006) Atrophy, hypertrophy and hypoxemia induce transcriptional regulators of the ubiquitin proteasome system in the rat heart. Biochem. Biophys. Res. Commun.. 342:361-364.
- Sharma, S., Dewald, O., Adrogue, J., Razeghi, P., Salazar, R.L., Crapo, J.D., Bowler, R.P., Entman, M.L., Taegtmeyer, H. (2006) Induction of antioxidant gene expression in a mouse model of ischemic cardiomyopathy is dependent on reactive oxygen species. Free Radic. Biol. Med. 40:2223-2231.
- Leichman, J.G., Aguilar, D., King, T.M., Vlada, A., Reyes, M., Taegtmeyer, H. (2006) An association of plasma free fatty acids and left ventricular diastolic function in patients with clinically severe obesity. Am. J. Clin. Nutr.. 84:336-341.
- Razeghi, P., Volpini, K.C., Wang, M-E., Youker, K.A., Stepkowski, S., Polonsky, K.S., Taegtmeyer, H. (2006) Mechanical unloading of the heart activates the calpain system. J. Mol. Cell Cardiol.. Oct 6 (electronic publish ahead of print).
- Leichman, J., Aguilar, D., Mehta, S., Scarborough, T., Wilson, E.B., Taegtmeyer, H. (2006) Improvements in systemic metabolism, anthropometrics, and left ventricular geometry three months after bariatric surgery. Surg. Obesity Rel. Dis. 2:592-599.
- Razeghi, P., Buksinska-Lisik, M., Palanichamy, N., Stepkowski, S., Frazier, O.H., Taegtmeyer, H. (2006) Transcriptional regulators of ribosomal biogenesis are increased in the unloaded heart. FASEB J 20:1090-1096
Heinrich Taegtmeyer, M.D., Ph.D.
Professor
UTHSC-Medical School, (713) 500 - 6569
Heinrich.Taegtmeyer@uth.tmc.edu
Metabolic regulation of cardiac gene expression
We examine the dynamics of energy transfer and of alterations in work load on gene expression of the heart. At the molecular level, we study mechanisms by which metabolically generated signals regulate signaling pathways of cardiac growth, including the expression of cardiac specific genes. To accomplish this goal, we make use of a variety of models, including the hypertrophied and atrophied heart in vivo, isolated working hearts, and isolated heart muscle cells in culture. At the clinical level we study molecular mechanisms of heart failure and the effects of diabetes and obesity on the heart. Here we make use of an extensive clinical data base and heart muscle samples generated in the course of implantation of left ventricular assist devices and at transplantation of failing human hearts. In separate studies we examine the cardiovascular consequences of severe obesity in patients and in rodent models.
A tutorial in my laboratory includes an introduction to a variety of techniques, including small animal surgery, perfusion techniques of the heart, isolation of neonatal and adult cardiac myocytes, tracer methods to study metabolic fluxes, measurements of metabolites, hormones and enzyme activities, as well as an assessment of metabolic activities, quantitative RT-PCR, immunoblotting, immunoprecipitation, and electrophoretic mobility shift assays. There are weekly lab seminars and lab meetings.
