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Int. J. Mol. Sci. 2017, 18(7), 1421; doi:10.3390/ijms18071421

Lipotoxicity-Induced PRMT1 Exacerbates Mesangial Cell Apoptosis via Endoplasmic Reticulum Stress

1
Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
2
Department of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science, Seoul National University, Seoul 08826, Korea
3
BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National University, Seoul 08826, Korea
4
Life Science Institutes, University of Michigan, Ann Arbor, MI 48109, USA
*
Author to whom correspondence should be addressed.
Received: 7 June 2017 / Revised: 22 June 2017 / Accepted: 29 June 2017 / Published: 3 July 2017
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Lipotoxicity-induced mesangial cell apoptosis is implicated in the exacerbation of diabetic nephropathy (DN). Protein arginine methyltransferases (PRMTs) have been known to regulate a variety of biological functions. Recently, it was reported that PRMT1 expression is increased in proximal tubule cells under diabetic conditions. However, their roles in mesangial cells remain unexplored. Thus, we examined the pathophysiological roles of PRMTs in mesangial cell apoptosis. Treatment with palmitate, which mimics cellular lipotoxicity, induced mesangial cell apoptosis via protein kinase RNA-like endoplasmic reticulum kinase (PERK) and ATF6-mediated endoplasmic reticulum (ER) stress signaling. Palmitate treatment increased PRMT1 expression and activity in mesangial cells as well. Moreover, palmitate-induced ER stress activation and mesangial cell apoptosis was diminished by PRMT1 knockdown. In the mice study, high fat diet-induced glomerular apoptosis was attenuated in PRMT1 haploinsufficient mice. Together, these results provide evidence that lipotoxicity-induced PRMT1 expression promotes ER stress-mediated mesangial cell apoptosis. Strategies to regulate PRMT1 expression or activity could be used to prevent the exacerbation of DN. View Full-Text
Keywords: PRMT1; lipotoxicity; mesangial cell; apoptosis; ER stress PRMT1; lipotoxicity; mesangial cell; apoptosis; ER stress
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Park, M.-J.; Han, H.J.; Kim, D.-I. Lipotoxicity-Induced PRMT1 Exacerbates Mesangial Cell Apoptosis via Endoplasmic Reticulum Stress. Int. J. Mol. Sci. 2017, 18, 1421.

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