XiaoYong Tong

Assistant Professor

Education:

Ph.D., Chinese Academy of Medical Science & Peking Union Medical College

General field of research:

Vascular Biology

Affiliations other than medicine:

Evans Center for Interdisciplinary Biomedical Research

Contact information:

Office
650 Albany street, X720
Phone: (617)-414 1009

Lab
650 Albany street, X720
Phone: (617)-638 7116

xytong@bu.edu

Keywords:

Smooth muscle cell; Atherosclerosis; SERCA; Nitric oxide

Summary of research interest:

Diabetic patients have much higher morbidity and mortality of cardiovascular diseases including atherosclerosis and restenosis compared with other populations. Vascular smooth muscle cell (SMC) migration contributes significantly to these pathological processes. Generally SMCs stay quiescent in vasculature. When the endothelium layer is disrupted, the underlying SMCs migrate from media to intima and form the neointima. This process is accelerated in diabetes mellitus (DM). Nitric oxide (NO), the biologically active component of endothelium-derived relaxing factor, has critical roles in the maintenance of vascular homeostasis. Previous studies showed that NO reduces intracellular calcium, which causes relaxation and inhibits SMC growth and proliferation in native smooth muscle. Sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) plays a very important role in maintaining intracellular calcium level by uptaking calcium into SR/ER. Our previous studies showed that NO upregulated SERCA activity by S-glutathiolation of the most reactive thiol on cysteine-674 (C674) and inhibited SMC migration. My major focus is to study the mechanisms of cardiovascular dysfunction in diabetes, mainly focus on SERCA, NADPH oxidase and smooth muscle cell migration. Those studies can also be expanded to obesity, insulin resistance and metabolic symptoms.

Recent publications:

Tong X, Porter LM, Liu G, Dhar-Chowdhury P, Srivastava S, Pountney DJ, Yoshida H, Artman M, Fishman GI, Yu C, Iyer R, Morley GE, Gutstein DE, Coetzee WA.  2006. Consequences of cardiac myocyte-specific ablation of KATP channels in transgenic mice expressing dominant negative Kir6 subunits. Am J Physiol Heart Circ Physiol. 291(2): H543-51. PMID: 16501027

Ying J, Tong XY, Pimental D, Weisbrod R, Trucillo MP, Adachi T, Cohen R.  2007. Cysteine-674 of the sarco/endoplasmic reticulum calcium ATPase is required for the inhibition of cell migration by nitric oxide. Arterioscler Thromb Vasc Biol. 27(4):783-90. PMID: 17234728

Malester B*, Tong XY*, Ghui I, Xu J, Hendricks-Munoz KD and Coetzee WA.  2007. Transgenic disruption of endothelial KATP channels in the mouse: effects on coronary flow mediated by altered endothelin-1 release. FASEB J. 21(9):2162-72. PMID: 17341678

Tong X*, Ying J, Pimentel DR, Trucillo M, Adachi T, Cohen RA.  2008. High glucose oxidizes SERCA cysteine-674 and prevents inhibition by nitric oxide of smooth muscle cell migration. J Mol Cell Cardiol. 44: 361-369. PMID: 18164028

Lancel S, Zhang J, Evangelista A, Trucillo M, Tong XY, Siwik D, Cohen RA and Colucci WS.  2009. Nitroxyl anion activates SERCA in cardiac myocytes via glutathiolation of cysteine 674. Cir Res. 104(6):720-3. PMID: 19265039

Technologies available for sharing upon request:

Biotin-IAM label of SERCA;  Rat and mouse aorta smooth muscle cell primary culture; Rat common carotid artery injury; Smooth muscle cell migration