Additional Contact Information:
Chair/Professor, Department of Biomedical Sciences
Physiologist, James H. Quillen VA Medical Center
Office B-110/B-208, Lab B150
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
Chair and 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
Senior Research Associate, Dept. of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA
Post-Doctoral Fellow, Human Genetics Section, Dept of Biology, McGill University, Montreal, Canada
Ph.D. College of Basic Sciences, Haryana Agril University, India
CARDIOVASCULAR SIGNALING AND PHYSIOLOGY
Main focus of my lab is to investigate 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. Myocardial infarction, isoproterenol infusion and ischemia/reperfusion are used as models of myocardial remodeling. Structural and functional parameters of the heart in mice are measured using echocardiography. Molecular and pharmacological approaches are used to investigate the signaling pathways using cardiac myocytes, fibroblasts and inflammatory cells. CardioGenomics and Proteomics approaches are used to understand the molecular basis of heart failure.Current Research Interests:
- Understanding the role of exogenous ubiquitin in myocardial ischemia/reperfusion injury.
- Understanding the role of ATM (ataxia telangiectasia mutated kinase) in heart disease.
- Investigation of the role of osteopontin, also called cytokine eta-1, in cardiac myocyte
apoptosis, collagen deposition and myocardial remodeling.
Suman Dalal, Ph.D., Assistant Professor (Collaborator), Dept of Health Sciences
Cerrone Foster, Ph.D., Associate Professor (Collaborator), Dept of Biological Sciences
Paige Shook, Graduate Student
Paulina Ramirez, Undergradute Honors Student
Barbara Connelly, Lab Coordinator
Department of Veterans Affairs
National Institutes of Health (NHLBI)
Wingard MC, Dalal S, Shook PL, Myers R, Connelly BA, Thewke DP, Singh M, Singh K. Deficiency of ataxia-telangiectasia mutated kinase modulates functional and biochemical parameters of the heart in response to Western-type diet. Am J Physiol Heart Circ Physiol. 2021;320(6):H2324-H2338. PMID: 33929897.
Dalal, S., Daniels, C.R., Li, Y., Wright, G.L., Singh, M., Singh, K. Exogenous ubiquitin attenuates hypoxia/reoxygenation-induced cardiac myocyte apoptosis via the involvement of CXCR4 and modulation of mitochondrial homeostasis. Biochem Cell Biol. 2020; 98:492-501.
Wingard, M.C., Frasier, C.R., Singh, M., Singh, K. Heart failure and diabetes: role of ATM. Curr Opin pharmacol. 2020; 54:27-35 (Invited review).
Dalal, S., Shook P.L., Singh, M. Singh, K. Cardioprotective potential of exogenous ubiquitin. Cardiovasc Drugs and Ther. 2020;54:27-35. PMID: 32745970 (Invited Review).
Scofield SLC, Dalal s, Lim K, Thrasher PR, Daniels CR, Peterson JM, Singh M, Singh K. Exogenous ubiquitin reduces inflammatory response and preserves myocardial function 3 days post-ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2019; 316:H617-628 (Article published with an editorial. The role of ubiquitin in cardiac ischemia-reperfusion injury. Kobayashi M, Higa JK, Matsui T. Am J Physiol Heart Circ Physiol. 2019; 316:H583-585).
Dalal, S, Connelly, B, Singh, M, Singh, K. NF2 signaling pathway plays a pro-apoptotic role in β-adrenergic receptor stimulated cardiac myocyte apoptosis. PLOS One 2018; 13(4):e0196626.
Thrasher, PR, Scofield, SLC, Dalal, S, Crawford, CC, Singh M, Singh, K. Ataxia-telangiectasia mutated kinase deficiency impairs autophagic response early during myocardial infarction. Am J Physiol Heart Circ Physiol 2018; 315:H48-H57 (Article published with an editorial; Ataxia telangiectasia mutated kinase is an autophagic balancer at the onset of heart failure. Yoshioka J. Am J Physiol heart Circ Physiol 2018; Jul 1;315(1):H80-H82).
Dalal S, Zha, Q, Singh M, Singh, K. Osteopontin-stimulated apoptosis in cardiac myocytes involves oxidative stress and mitochondrial death pathway: role of a pro-apoptotic protein Bik. Mol. Cell. Biochem. 2016; 418:1-11.
Daniel LL, Scofield SLC, Thrasher P, Dalal S, Daniels CR, Foster CR, Singh M, Singh K. Ataxia Telangiectasia mutated kinase deficiency exacerbates left ventricular dysfunction and remodeling late after myocardial infarction. AJP Heart and Circulatory Physiology 2016; 311:455-452.
Scofield, L.C., Amin, P., Singh, M., Singh, K. Extracellular ubiquitin: role in myocyte apoptosis and myocardial remodeling. Comprehensive Physiology, 2015: 15;6:527-60 (Invited Review).
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).
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., 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.
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.
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 β-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)
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: 303:H1459-H1468.