Mohan, SumathyGraduate School of Biomedical Sciences |
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| 9/2016 - Present | Professor/Research and . | University of Texas Health Science Center, Pathology |
| Year | Degree | Discipline | Institution |
| 1995 | PhD | Biochemical Genetics | P.G. Inst. of Basic Medical Sciences, University of Madras India |
| 1995 | Postdoctoral Training | Biochemical Genetics | University of Madras Madras , India |
| 1981 | MS | Biochemistry | P.G. Inst. of Basic Medical Sciences, University of Madras India |
| 1979 | BS | Biochemistry | Avinashilingam Home Science College, University of Madras India |
| Postdoctoral Training | Applied Mechanics in Biomedical Res. Application | Indian Institute of Technology Madras , India |
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| Postdoctoral Training | Biochemical Genetics | Bureau of Police Research and Development Madras , India |
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| Postdoctoral Fellowship | Microbiology | University of Texas Health Science Center at San Antonio San Antonio , TX |
Areas of Research Interest:- Atherosclerotic lesions typically occur in areas of low shear flow regions. The mechanisms involved in developing these lesions are poorly understood. My long-term goal is first to identify molecular targets. Once this is accomplished it will then be possible to develop strategies for novel interventional procedures and agents to control the development of the disease. I have been studying endothelial cell biology in health and disease, in particular its responses and gene expression under conditions that influence the atherogeneic process. I have several years of experience in in vitro studies in which human vascular endothelial cells are maintained under flow shear stress, which simulate a tissue microenvironment mimicking the in vivo conditions. I have long standing interest in examining the alterations in the nuclear factor kappa B regulation under conditions of shear stress which promotes the endothelial cells to be ?activated? thus favoring the atherogenic process. Recently, I extended my expertise in the area of diabetes-research to explore similar possible mechanisms that contribute to accelerated-atherosclerosis in diabetic arteries. These studies reported from my laboratory have demonstrated the profound involvement of endothelial nitric oxide synthase under hyperglycemic conditions. My current studies are focused toward determining how the balance of activities of Inhibitor kappa B kinase and endothelial nitric oxide synthase reflect oxidative stress responses of endothelial cells that are induced by high glucose. Also, the recent generation of a double knockout mouse model (eNOS knockout mouse with a diabetic background) and Transgenic- diabetic model in my laboratory will illuminate some of these basic mechanisms in vivo and identify components that cause endothelial dysfunction. In addition to its application to characterize the pathology of vasculature caused by depletion of eNOS, the severe lesions of the kidney found in these mice will provide a strong basis to consider this strain as an excellent diabetic nephropathy model. This diabetic mouse model will also be used to examine the contribution of endothelial progenitor cells in vascular repair mechanisms in response to mechanical/radiation injury that results in endothelial denudation. |
| Date | Description | Institution | # Students |
| 10/2018 - Present | Membership on Supervising Committee | UT Health Science Center | |
| 9/2017 - Present | Post-Doctoral Student Supervision | UT Health Science Center | |
Abstract |
| Natarajan M, Manickam K, Koropinski R, Baha A, Gaudett C, Janardhanan P, Mohan S. Inhibitor Kappa B Kinase regulates nitric oxide synthase activity in vascular endothelial cells; 2014 Jan. (Atherosclerosis Thrombosis Vascular Biology). |
| Manickam K, Janardhanan P, Gaudett C, Reddick RL, Haperen RV, Mohan N, Mohan S. Improved vasodialotory function in Ins2 Akita type-1 diabetic mice with daily intake of oral L-Arginine in combination with salsalate; 2014 Jan. (Atherosclerosis Thrombosis Vascular Biology). |
Journal Article |
| Sumathy Mohan1, Natarajan Mohan1 Robert L. Reddick1 Krishnan Manickam1, Kathy Woodruff1, Diane Horn1, Samy Habib2, Rene de Crom 3, and Sherry L. Werner. Overexpression of endothelial nitric oxide synthase on a Ins2Akita-type-1 diabetic background exacerbates kidney injury J of Diabetes & its complications 2019 Jan;:23-32. |
| Al-Obaidi N1, Mohan S2, Liang S1, Zhao Z1, Nayak BK1, Li B3, Sriramarao P4, Habib SL1,5. Galectin-1 is a new fibrosis protein in type 1 and type 2 diabetes FASEB 2019 Jan;10(1096). |
| Sureshkumar MA, Delma CR, Liang S, Zhao Z, Nayak BK, Li B, Sriramarao P, Habib SL, Natarajan M. Heterozygous Tsc2 (Tsc2 /-) mouse model to study induced renal cancer in response to ionizing radiation in low doses Carcinogenesis 2018 Dec;. |
| Natarajan, M, Aravindan N, Sprague EA and Mohan S. Hemodynamic Flow-induced Mechanotransduction Signaling Influences Radiation Response of Vascular Endothelium (In Press) Radiat Res 2016 Jul;. |
| *Chandra SB, *Mohan S, Ford BM, Huang L, Janardhanan P, Deo KS, Cong L, Muir ER, Duong TQ. Targeted overexpression of endothelial nitric oxide synthase in endothelial cells improves cerebrovascular reactivity in Ins2Akita-type-1 diabetic mice Journal of Cerebral Blood Flow and Metabolism *Both authors contributed equally 2016 Jun;36(6):1135-1142. |
| Krishnan M, Janardhanan P, Roman L, Reddick RL, Natarajan M, van Haperen R, Habib SL, de Crom R, Mohan S. Enhancing eNOS activity with simultaneous inhibition of IKKB restores vascular function in Ins2Akita /- type-1 diabetic mice Lab Invest 2015 Oct;95(10):1092-104. |
| Natarajan M, Konopinski R, Krishnan M, Roman L, Bera A, Hongying Z, Habib S, Mohan S. Inhibitor kappa B kinase attenuates Hsp90-dependent endothelial nitric oxide synthase function in vascular endothelial cells Am J Physiol Cell Physiol 2015 Apr;308(8):C673-83. |
| Adam K, Hung-1 C, Mohan S, Sitai L, Yidong C, Habib SL. Microarray profile of human kidney from diabetes, renal cell carcinoma and renal cell carcinoma with diabetes Genes & Cancer 2015 Jan;6(1-2). |
| Habib SL, Mohan S, Liang S, Li B, Yadav M. Novel mechanism of transcriptional regulation of cell matrix protein through CREB Cell Cycle 2015 Jan;14(16):2598-608. |
| Ghosh S, Lertwattanarak R, Gardu?o J, Galeana JJ, Li J, Zamarripa F, Lancaster JL, Mohan S, Hussey S, Musi N. Elevated Muscle TLR4 Expression and Metabolic Endotoxemia in Human Aging J. Gerontol A Biol Sci Med Sci 2014 May;70(2):232-46. |
| Yeh CK, Harris SE, Mohan S, Horn D, Fajardo R, Chun YHP, Jorgensen J, MacDougall M, Werner SA. Hyperglycemia and Xerostomia are key determinants of tooth decay in Type 1 diabetic mice Lab Invest 2012 Jun;92(6):868-882. |
| Wittrant Y, Gorin Y, Mohan S, Wagner B, Abboud-Werner SL. Colony-stimulating factor-1 (CSF-1) directly inhibits receptor activator of nuclear factor-{kappa}B ligand (RANKL) expression by osteoblasts Endocrinology 2009 Nov;150(11):4977-4988. |
Federal |
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| Funding Agency | NIH |
| Title | Dysfunction of retinal neurons and circuits early in diabetic retinopathy. |
| Status | Complete |
| Period | 5/2014 - 4/2019 |
| Role | Co-Investigator |
| Grant Detail | To determine VEAFaction in Retinal endothelial cells under the influence of high glucose |
| Funding Agency | VA MERIT |
| Title | Diabetic Complications and Risk of Kidney Cancer |
| Status | Complete |
| Period | 6/2014 - 5/2018 |
| Role | Co-Investigator |
| Grant Detail | Screening of type-2 diabetic db/db mice among Tsc2++/TSC 2+/- mice. |
| Funding Agency | NIH |
| Title | Influence of High Glucose on Endothelial Function |
| Status | Complete |
| Period | 7/2012 - 6/2017 |
| Role | Principal Investigator |
| Grant Detail | The major goal is to understand the mechanism of endothelial dysfunction in Type-1 diabeties. |
State |
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| Funding Agency | San Antonio Area Foundation |
| Title | Diabetes, Aging and Endothelial Dysfunction |
| Status | Active |
| Period | 4/2019 - 9/2020 |
| Role | Principal Investigator |
| Grant Detail | |