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Biomedical Sciences

Quillen College of Medicine

Krishna Singh
Krishna Singh

Krishna  Singh 

Biomedical Sciences






Additional Contact Information:

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)
Office  B-110, Lab B150
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 70582
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


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


Singh lab members

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.


Suman Dalal, Postdoctoral Fellow
Stephanie Scofield, Graduate student
Patsy Thrasher, Graduate Student
Barbara Connelly; B.A.; Lab Coordinator


Department of Veterans Affairs
National Institute of Health (NHLBI)


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).

Singh, M., Foster, C., Dalal, S., Singh, K. Osteopontin: role in extracellular matrix deposition and myocardial remodeling post-MI. J. Mol. Cell. Cardiol. 2010, 48(3):538-43.

Singh, M., Foster, C., Dalal, S., Singh, K. Role of osteopontin in heart failure associated with aging. Heart Fail Rev. 2010,15(5):487-94.

Ha, T., Lu, C., Liu, L., Hua, F., Hu, Y., Kelley, J., Singh, K., Kao, R.L., Kalbfleisch, J., Williams, D.L., Li, C. TLR2 ligands attenuate cardiac dysfunction in polymicrobial sepsis via a phosphoinositide 3-kinase dependent mechanism. Am. J. Physiol. Heart and Circulatory Physiol. 2010, 298(3):H984-H991.

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.

Amin, P., Singh, M., Singh, K. -adrenergic receptor-stimulated cardiac myocyte apoptosis: Role of 1 integrins. J. Signal Transduction. Volume 2011, Article ID 179057, 9 pages doi:10.1155/2011/179057.

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

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 -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)

Gao, M., Ha, T., Zhang, X., Liu, L., Wang, X., Kelley, J., Singh, K., Kao, R., Gao, X., Williams, D., Li, C. Toll-like receptor 3 plays a central role in cardiac dysfunction during polymicrobial sepsis. Critical Care Medicine 2012, 40:2390-2399. (Article published with an editorial; Not only a toll for viruses: the role of toll-like receptor 3 in nonviral sepsis-induced cardiac depression. Michael, P., Bleiblo, F., Kumar, A., Kumar, A. Critical Care Medicine 2012, 40: 2514-2514).

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.

Li, C., Hua, F., Ha, T., Singh, K., Lu, C., Kalbfleisch, J., Breuel, K.F., Ford, T., Kao, R.L., Ozment-Skelton, T.R., Williams, D.L. Activation of myocardial phosphoinositide-3-kinase p110 ameliorates cardiac dysfunction and improves survival in murine sepsis. PLoS ONE, 2012: 7(9):e44712.

Daniels, C.R., Foster, C., Yakoob, S., Dalal, S., Joyner, W.L., Singh, M., Singh, K. Exogenous ubiquitin modulates chronic -adrenergic receptor stimulated myocardial remodeling: role in Akt activity and matrix metalloproteinase expression. Am. J. Physiol. Heart and Circ. Physiol. 2012: 303:H1459-H1468.

Gao, M., Ha, T., Zhang, X., Wang, X., Liu, L., Kalbfleisch, J., Singh, K., Williams, D., Li, C. The toll-like receptor 9 ligand, CpG oligonucleotide, attenuates cardiac dysfunction in polymicrobial sepsis, involving activation of both phosphoinositide 3 kinase/Akt and extracellular-signal-related kinase signaling. J. Infect. Dis. 2013: 207:1471-1479.

Foster, C.R., Daniel, L.L., Daniels, C.R., Dalal, S., Singh, M., Singh, K. Deficiency of ataxia telangiectasia mutated kinase modulates cardiac remodeling following myocardial infarction: involvement in fibrosis and apoptosis. PLoS One; 2013; 8(12):e83513.

Steagall R.J. Daniels, C.R., Dalal, S., Joyner, W.L., Singh, M., Singh, K. Extracellular ubiquitin increases expression of angiogenic molecules and stimulates angiogenesis in cardiac microvascular endothelial cells. Microcirculation 2014; 21:324-332 (Special Issue: Angiogenesis: Growth Points).

Cooper, D.L., Murrell, D.K., Conder, C.M., Palau, V.P., Campbell, G.E., Lynch, S.P., Denham, J.W., Hanley, A.V., Bullins, K.W., Panus, P.C., Singh, K., Harirforoosh, S. Exacerbation of Celecoxib-Induced Renal Injury by Concomitant Administration of Misoprostol in Rats. PLoS One, 2014; 9(2):e89087.

Dalal, S., Zha, Q, Daniels, C.R., Steagall, R.J., Joyner, W.L., Gadeau, A-P., Singh, M., Singh, K. Osteopontin stimulates apoptosis in adult cardiac myocytes via the involvement of CD44 receptors, mitochondrial death pathway and endoplasmic reticulum stress. Am J. Physiol. Heart and Circ Physiol. 2014; 306:H1182-H1191. 

Daniel L.L., Joyner, W.L., Singh, M., Singh, K. Integrins: implications for aging and heart failure therapy. In: Aging and Heart Failure, Jugdutt B (Ed.). Springer Publishing Co., 2014; 401-410.

Singh, M., Dalal, S., Singh, K. Osteopontin: at the cross-roads of myocyte survival and myocardial function. Life Sci. 2014; 118:1-6.

Daniel, L.L., Daniels, C.R., Harirforoosh, S., Foster, C.R., Singh, M., Singh, K. Deficiency of ataxia telangiectasia mutated kinase delays inflammatory response in the heart following myocardial infarction. J Am Heart Assoc. 2014;3(6):e001286 (Article published with an editorial. Ataxia-telangiectasia mutated kinase: a potential new target for suppressing inflammation in heart failure? Kukreja, C. J Am Heart Assoc. 2014;3(6):e001591.

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