- Ph.D., University of Nebraska Medical Center (1999)
- M.S., Anhui Medical University, China (1989)
- B.S., Anhui Medical University, China (1983)
The global objective of my research program is to investigate Ca2+ signaling in kidney cells and vascular smooth muscle cells under both physiological and pathological conditions. The major goal of my projects is to delineate the molecular and cellular mechanisms for regulation of glomerular function and vascular tone by TRPC channels and store-operated Ca2+ channels, and the implications of these channels in renal and vascular complications in diabetes. These studies are being conducted in cultured cells, in isolated animal tissues, and in intact animal models. Three major research interests were focused during the period under the post-tenure review.
Kidney function, glomerular mesangial cell, store-operated calcium channel, TRPC channel, diabetic kidney disease
Store-operated Ca2+ channel and diabetic kidney disease We have demonstrated that store-operated Ca2+ channel decreases glomerular ECM protein production by mesangial cells. Ongoing research is directed toward defining molecular mechanisms by which store-operated Ca2+ channel in mesangial cells inhibits fibrotic response in glomerulus. We will continue our collaborations with Dr. Davis group in Caltech and Dr. Mathis at ICMD of UNTHSC to further investigate how the renoprotective store-operated Ca2+ channel is involved in the development of DN. We will focus two signaling pathways, TGF-β1/Smad3 signaling pathway and cytokines/chemokines/inflammatory pathways.
Inhibitor of myogenic family isoform a (I-mfa) and diabetic kidney disease I-mfa is a cytosolic protein, originally identified as a protein interacting with MyoD. We recently found that I-mfa is an inhibitor of store-operated Ca2+ channel. We have shown that inhibition of store-operated Ca2+ channel in mesangial cells can increase glomerular ECM protein contents. In addition, I-mfa can increase abundance of cytosolic β-catenin. Activation of the Wnt/β-catenin signaling plays an important role in the pathogenesis and progression of DN. Therefore, I-mfa may be an adverse factor to stimulate the development of DN. One of our ongoing projects is to investigate whether and how I-mfa contributes to renal injury in diabetes. This study will be conducted in collaborations with Dr. Davis in Caltech and Dr. Leonidas Tsiokas at University of Oklahoma Health Sciences Center.
- NIH/NIDDK (1RO1DK115424), “Store-operated Ca2+ signaling in kidney glomerular mesangial cells”, 12/01/2017-11/30/2021, $1,314,000 (PI)
- American Heart Association (20TPA35500045), A new mechanism for glomerular hyperfiltration at early stage of renal microvascular complication of diabetes mellitus. 1/1/21-12/31/23, $300,000 (PI)
- Ma R, Smith S, Child A, Carmines PK and Sansom SC. Store-operated calcium channels in human mesangial cells. Am J Physiol Renal Physiol. 278: F954-F961, 2000 (PMID: 10836983).
- Ma R and Sansom SC. Epidermal growth factor activates store-operated calcium channel in human glomerular mesangial cells. J Am Soc Nephrol 12:47-53, 2001 (PMID: 11134249).
- Li WP, Tsiokas L, Sansom SC and Ma R. Epidermal growth factor activates store-operated Ca2+ channels through an IP3 independent pathway in human glomerular mesangial cells. J Biol Chem 279:4570-4577, 2004 (PMID: 14612458).
- Wu P, Ren Y, Ma Y, Wang Y, Jiang H, Chaudhari S, Davis ME, Zuckerman JE and Ma R. Negative regulation of Smad1 pathway and collagen IV expression by store-operated Ca2+ entry in glomerular mesangial cells. Am J Physiol Renal Physiol 312: F1090-F1100, 2017 (PMCID: PMC5495888).
- Ma R, Pluznick JL, Kudlacek PE and Sansom SC. Protein kinase C activates store-operated Ca2+ channels in human glomerular mesangial cells. J Biol Chem 276: 25759-25765, 2001 (PMID: 11352899).
- Ma R, Kudlacek PE and Sansom SC. Protein kinase C participates in activation of store-operated Ca2+ channels in human mesangial cells. Am J Physiol Cell Physiol 283:C1390-1398, 2002 (PMID: 12372800).
- Ma R, Rundle D, Jacks J, Koch M, Downs T and Tsiokas L. Inhibitor of myogenic family: a novel suppressor of store-operated Ca2+ currents through an interaction with TRPC1. J Biol Chem 278:52763-52772, 2003 (PMID: 14530267).
- Sours-Brothers S, Ding M, Graham S and Ma R. Interaction between TRPC1/TRPC4 assembly and STIM1 contributes to store-operated Ca2+ entry in mesangial cells. Exp Biol Med 234:673-682, 2009 (PMID: 19307462).
- Wu P, Wang Y, Davis ME, Zuckerman JE, Chaudhari S, Begg M and Ma R. Store-operated Ca2+ channel in mesangial cells inhibits matrix protein expression. J Am Soc Nephrol 26: 2691-2702, 2015 (PMCID: PMC4625675).
- Chaudhari S, Wu P, Wang Y, Ding Y, Yuan J and Ma R. High glucose and diabetes enhanced store-operated Ca2+ entry and increased expression of its signaling proteins in mesangial cells. Am J Physiol Renal Physiol 306: F1069-F1080, 2014 (PMCID: PMC4010683).
- Chaudhari S, Li W, Wang Y, Jiang H, Ma Y, Davis ME, Zuckerman JE, and Ma R. Store-operated calcium entry suppressed TGFβ1-Smad3 signaling pathway in glomerular mesangial cells. Am J Physiol Renal Physiol 313: F729-F739, 2017 (PMCID: PMC5625109)
- Jiang H, Zou S, Chaudhari S, and Ma R. Short term high glucose treatment decreased abundance of Orai1 protein through posttranslational mechanisms in rat mesangial cells. Am J Physiol Renal Physiol 314: F855-F863, 2018 (PMCID: PMC6031918).
- Sours S, Du J, Chu S, Zhou XJ, Ding M and Ma R. Expression of canonical transient receptor potential (TRPC) proteins in human glomerular mesangial cells. Am J Physiol Renal Physiol 290:F1507-F1515, 2006 (PMID: 16418302).
- Du J, Sours-Brothers S, Coleman R, Ding M, Graham S, Kong D and Ma R. TRPC1 channel is involved in contractile function of glomerular mesangial cells.J Am Soc Nephrol 18:1437-1445, 2007 (PMID: 1738936).
- Graham S, Ding M, Sours-Brothers S, Yorio T and Ma R. Downregulation of TRPC6 protein expression by high glucose, a possible mechanism for the impaired Ca2+ signaling in glomerular mesangial cells in diabetes. Am J Physiol Renal Physiol 293: F1381-F1390, 2007 (PMID: 17699555).
- Li WZ, Ding Y, Smedley C, Wang Y, Chaudhari S, Birnbaumer L, and Ma R. Increased glomerular filtration rate and impaired contractile function of mesangial cells in TRPC6 knockout mice. Sci Rep 7: 4145, 2017 (PMCID: PMC5482875).
- Graham S, Ding M, Ding Y, Sours-Brothers S, Luchowski R, Gryczynski Z, Yorio T, Ma H and Ma R. Canonical transient receptor potential 6 (TRPC6), a redox-regulated cation channel. J Biol Chem 285:23466-23476, 2010 (PMCID: PMC2906337).
- Graham S, Gorin Y, Abboud HE, Ding M, Lee DY, Shi H, Ding Y and Ma R. Abundance of TRPC6 protein in glomerular mesangial cells is decreased by ROS and PKC in diabetes. Am J Physiol Cell Physiol 301:C304-C315, 2011 (PMCID: PMC3154551).
- Ding Y, Winters A, Ding M, Graham S, Akopova I, Muallem S, Hong JH, Gryczynski Z, Yang SH, Birnbaumer L and Ma R. Reactive oxygen species-mediated TRPC6 activation in vascular myocytes, a mechanism for vasoconstrictor-regulated vascular tone. J Biol Chem 286:31799-31809, 2011 (PMCID: PMC3173128).
- Wang Y, Ding M, Chaudhari S, Ding Y, Yuan J, Stankowska D, He S, Krishnamoorthy R, Cunningham JT and Ma R. NF-κB mediates suppression of canonical transient receptor potential 6 (TRPC6) expression by ROS and PKC in kidney cells. J Biol Chem 288:12852-12865, 2013 (PMCID: PMC3642329).
- Click here for a complete list of publications (http://www.ncbi.nlm.nih.gov/sites/myncbi/1tsU8oCJViFkE/bibliography/41689518/public/?sort=date&direction=ascending)
- Renal Physiology
- Cell Physiology
UNTHSC Committees and Service
- Faculty grievance and appeal committee
- P&T committee of GSBS