References:
- Razeghi P, Baskin KK, Sharma S, Young ME, 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 RL, Crapo JD, Bowler RP, Entman ML, 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 JG, Aguilar D, King TM, 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 KC, Wang M-E, Youker KA, Stepkowski S, Polonsky KS, 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 EB, 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 OH, 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.
