Dr. Krishna Singh


Dr. Krishna Singh
Dr. Krishna Singh, Professor

Contact Information:

Professor, Department of Biomedical Sciences
Physiologist, James H Quillen VA Medical Center
James H. Quillen College of Medicine
PO Box 70582
Johnson City, TN 37614-1708
Stanton-Gerber Hall (VA 178)
Room B-110
Ph: 423-439-2049
Fax: 423-439-2052

Mail Address:
East Tennessee State University
James H. Quillen College of Medicine
Department of Biomedical Sciences
East Tennessee State University
P. O. Box 70,582
Johnson City, TN 37614


Street Address:
East Tennessee State University
James H. Quillen College of Medicine
Department of Biomedical Sciences 
Stanton-Gerber Hall Room B-110
178 Maple Avenue
Mountain Home, TN 37684


Education: 
 

Ph.D. College of Basic Sciences, Haryana Agril. University, India 

Post-doctoral Fellow, Human Genetics Section, Dept. of Biology, McGill University, Montreal, Canada 

Senior Research Associate, Dept. of Medicine, Brigham & Women’s Hospital, Harvard Medical School, Boston, MA 


Recent Academic Appointments:

Professor, Dept of Biomedical Sciences, East Tennessee State University, Johnson City, TN
Professor, Dept of Physiology, East Tennessee State University, Johnson City, TN
Physiologist, James H Quillen VA Medical Center, Mountain Home, TN
Associate Professor, Dept of Physiology, East Tennessee State University, Johnson City, TN
Assistant Professor (adjunct), Dept. of Biochemistry, Boston University School of Medicine, Boston, MA
Research Scientist, VA Medical Center, Boston, MA
Assistant Research Professor, Dept. of Medicine, Boston University School of Medicine, Boston, MA

Research Interests:

1- Cardiovascular Signaling
2- Cardiovascular Physiology
3- Pulmonary Physiology

The main focus of my lab is to study molecular and cellular basis of heart failure. The studies involve both in vivo and in vitro strategies. For in vivo experiments, we are using transgenic (gene knock-out) mice. Heart function is measured using Langendorff perfusion analysis, Millar catheter and echocardiography. Molecular and pharmacological approaches are used to study the signaling pathways in vitro using isolated cardiac myocytes, fibroblasts and microvascular endothelial cells. CardioGenomics and Proteomics approaches are used to understand the molecular basis of heart failure.  

One major project investigates the molecular signals involved in cardiac myocyte apoptosis and myocardial remodeling following beta-adrenergic receptor (b-AR) stimulation and myocardial infarction. Current research interests are-

1) Understanding the signaling pathways involved in anti-apoptotic effects of extracellular ubiquitin.

2) Elucidation of role of ATM (ataxia telangiectasia mutated kinase) in heart disease.

3) Understanding the role of endoplasmic reticulum (ER or sarcoplasmic reticulum in cardiac myocytes) stress in cardiac myocyte apoptosis and myocardial remodeling.

Other major project investigates the role of osteopontin, also called cytokine eta-1, in cardiac myocyte apoptosis, collagen deposition and myocardial remodeling.

Research Support:

Department of Veterans Affairs
National Institute of Health (NHLBI)

Lab Members:

Rebecca Steagall, Ph.D.; Research Associate
Suamn Dalal, M.S.; M.Phil; Research Scholar
Christopher R. Daniels; B.S.; Graduate Student
Laura L. Daniel; B.S.; Graduate Student
Barbara Connelly; B.A.; Lab Coordinator

Recent Publications:

1. Daniels, C.R., Foster, C., Yakoob, S., Dalal, S., Joyner, W.L., Singh, M., Singh, K. Exogenous ubiquitin modulates chronic β-adrenergic receptor stimulated myocardial remodeling: role in Akt activity and matrix metalloproteinase expression. Am. J. Physiol. Heart and Circ. Physiol. 2012 (In Press).

2. Steagall, R.J., Sipe, A, Williams, C.A., Joyner, W., Singh, K. Substance P release in response to cardiac ischemia from rat thoracic spinal dorsal horn is mediated by TRPV1. Neuroscience 2012, 214:106-119.

3. Foster, C.R., Zha, Q., Daniel, L.L., Singh, M., Singh, K. Lack of ataxia telangiectasia mutated kinase induces structural and functional changes in the heart: Role in b-adrenergic receptor-stimulated apoptosis. Exp Physiol . 2012, 97:506-515. ( Article published with a viewpoint; Ataxia telangiectasia mutated kinase in the heart: currency for myocyte apoptosis. Gorr, M.W., Stevens, S.C.W. and Wold, L.E. Exp Physiol . 2012, 97:476).

4. Dalal, S., Foster, C.R., Das, B.C., Singh, M., Singh, K. b-adrenergic receptor stimulation induces endoplasmic reticulum stress in cardiac myocytes: role in apoptosis. Mol Cell Biochem . 2012, 364:59-70.

5. Foster, C.R., Singh, M., Subramanian, V., Singh, K. Ataxia telangiectasia mutated kinase plays a protective role in beta-adrenergic receptor-stimulated cardiac myocyte apoptosis and myocardial remodeling. Mol. Cell. Biochem. 2011, 353:13-22.

6. Singh, M., Roginskaya, M., Dalal, S., Menon, B., Kaverina, E., Singh, K.  Extracellular ubiquitin inhibits beta-AR-stimulated apoptosis in cardiac myocytes:  role of GSK-3beta and mitochondrial pathways.  Cardiovasc. Res. 2010, 86:20-28 (Article published with an editorial; Ubiquitin, a novel paracrine messenger of cardiac cell survival. Li, D., and Depre, C. Cardiovasc Res. 2010, 86:1-3).

7. Krishnamurthy, P., Subramanian, V., Singh, M., Singh, K. β1 integrins modulate β-adrenergic receptor stimulated apoptosis and myocardial remodeling. Hypertension 2007, 49(4):865-72 (Article published with an editorial; Ionotropic Stress and Integrin: Another Link to Myocardial Remodeling. Pokharel, S and Sharma U.C. Hypertension 2007, 49:767-768).

8. Subramanian, V., Krishnamurthy, P., Singh, K., Singh, M. Lack of Osteopontin improves cardiac function in streptozotocin-induced diabetic mice. Am. J. Physiol. Heart and Circulatory Physiol. 2007, 292:H673-683.

9. Menon, B., Johnson, J.N., Ross, R.S., Singh, M., Singh, K. Glycogen synthase kinase-3β plays a pro-apoptotic role in β-adrenergic receptor-stimulated apoptosis in adult rat ventricular myocytes: role of β1 integrins. J. Mol. Cell. Cardiol. 2007, 42:653-661.

10. Trueblood, N., Xie, Z., Communal, C., Sam, F., Ngoy, S., Liaw, L., Wang, J., Sawyer, D.B., Bing, O.H.L., Apstein, C.S., Colucci, W.S., Singh, K. Exaggerated left ventricular dilation and reduced collagen deposition post myocardial infarction in mice lacking osteopontin. Circ. Res. 2001; 88:1080-1087 ( Cover Article ).