Qiang Tong, Ph.D.
Departments of Pediatrics, Medicine, Molecular Physiology & Biophysics, Baylor College of Medicine
1100 Bates Street, Room 7067
Tel: (713) 798-6716
B.S. Biology, University of Science and Technology of China
M.S. Cell Biology, Shanghai Institute of Cell Biology, Chinese Academy of Sciences
Ph.D. Biochemistry, Ohio State University
Postdoctoral Fellow, Nutrition, Harvard School of Public Health
Metabolic Regulation in Obesity, Diabetes and Aging
The main focus of our research is to study the molecular mechanism of caloric restriction, which extends animal life span and reduces the onset of obesity, diabetes, cancer, neurodegeneration and cardiovascular diseases. The study of the molecular mechanism of caloric restriction may lead to pharmaceutical treatments that may mimic caloric restriction’s beneficial effects. Sir2 gene, which encodes a NAD+-dependent protein deacetylase, was reported to mediate the effect of caloric restriction in yeast. We have demonstrated that the expressions of two of the seven mammalian Sir2 homologues, SIRT2 and SIRT3, are up-regulated in response to dietary restriction, cold exposure and oxidative stress. We have illustrated the molecular mechanism of SIRT2’s action in oxidative stress resistance and the inhibition of adipocyte formation. We have also shown how SIRT3 activates adaptive thermogenesis program in brown adipose tissue and how SIRT3 regulates glucose disposal and fat oxidation in skeletal muscle. To understand the underlying molecular mechanisms, we have identified several substrate proteins for SIRT2 and SIRT3. Research is under way to investigate the actions of sirtuins in gain or loss-of-function animal models.
Another research direction we take is to study the development of adipose tissue and its changes during obesity. By investigating how mature adipocytes are derived from multi-potent precursor cells, we can gain insight into obesity prevention. In addition, by studying how factors produced by adipocytes and adipose tissue influence whole body metabolism, we may learn how obesity causes insulin resistance and subsequent type-2 diabetes. We have revealed that the expression of the PU.1 transcription factor is increased by obesity in visceral but not subcutaneous adipose tissues. We further found that in adipocytes, PU.1 up-regulates the generation of free radicals and pro-inflammatory cytokines to suppress insulin signaling. We are currently exploring the possibility to ameliorate obesity-associated metabolic dysfunction by targeting the PU.1 pathway.
Qiang Tong, Gökhan Dalgin, Haiyan Xu, Chao-Nan Ting, Jeffrey M. Leiden and Gökhan S. Hotamisligil (2000) Function of GATA Transcription Factors in Preadipocyte-Adipocyte Transition. Science, Vol. 290, 134-138.
Qiang Tong, Judy Tsai, Guo Tan, Gökhan Dalgin, and Gökhan S. Hotamisligil (2005) Interaction Between GATA and the C/EBP Family of Transcription Factors is Critical in GATA-Mediated Suppression of Adipocyte Differentiation, Molecular and Cellular Biology, Vol. 25(2):706-715.
Tong Shi, Fei Wang, Emily Stieren, and Qiang Tong (2005) SIRT3, A Mitochondrial Sirtuin Deacetylase, Regulates Mitochondrial Function And Thermogenesis In Brown Adipocytes, The Journal of Biological Chemistry. 280(14):13560-13567.
Fei Wang, Margaret Nguyen, F. Xiao-Feng Qin, and Qiang Tong (2007) SIRT2 Deacetylates FOXO3a in Response to Oxidative Stress and Caloric Restriction. Aging Cell, 6:505-14.
Fei Wang and Qiang Tong (2008) Transcription Factor PU.1 Is Expressed in White Adipose and Inhibits Adipocyte Differentiation. Am J Physiol Cell Physiol, 295:C213-20.
Julia Skokowa, Dan Lan, Basant Kumar Thakur, Fei Wang, Kshama Gupta, Gunnar Cario, Annette Muller Brechlin, Axel Schambach, Lars Hinrichsen, Gustav Meyer, Matthias Gaestel, Martin Stanulla, Qiang Tong and Karl Welte (2009) NAMPT is essential for the G-CSF-induced myeloid differentiation via a NAD+-sirtuin-1-dependent pathway. Nat Med, 15:151-8.
Fei Wang and Qiang Tong (2009) SIRT2 Suppresses Adipocyte Differentiation by Deacetylating Foxo1 and Enhancing Foxo1’s Repressive Interaction with PPARγ. Mol. Biol. Cell, 20:801-8.
Orsolya M. Palacios, Juan J. Carmona, Shaday Michan, Ke Yun Chen, Yasuko Manabe, Jack Lee Ward III, Laurie J. Goodyear, and Qiang Tong (2009) Diet and exercise signals regulate SIRT3 and activate AMPK and PGC-1α, in skeletal muscle, Aging, 1:771-783.
Yongjie Yang, Huseyin Cimen, Min-Joon Han, Tong Shi, Jian-Hong Deng, Hasan Koc, Orsolya M. Palacios, Laura Montier, Yidong Bai, Qiang Tong* and Emine C. Koc* (2010) NAD+-dependent deacetylase SIRT3 regulates mitochondrial protein synthesis by deacetylation of the ribosomal protein MRPL10. J Biol Chem. 285:7417-7429 (*co-corresponding authors)
Yongjie Yang, Basil P. Hubbard, David A. Sinclair, Qiang Tong (2010) Characterization of murine SIRT3 transcript variants and corresponding protein products. J Cell Biochem. 111(4):1051-8.
Fei Wang, Chia-Hsin Chan, Keyun Chen, Xinfu Guan, Hui-Kuan Lin, Qiang Tong (2011) Deacetylation of FOXO3 by SIRT1 or SIRT2 Leads to Skp2-Mediated FOXO3 Ubiquitination and Degradation. Oncogene, 31:1546–1557.
Ligen Lin, Weijun Pang, Keyun Chen, Fei Wang, Jon Gengler, Yuxiang Sun, and Qiang Tong (2012) Adipocyte Expression of PU.1 Transcription Factor Causes Insulin Resistance through Up-regulation of Inflammatory Cytokine Gene Expression and ROS Production. Am J Physiol-Endocrinology and Metabolism, in press