Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells.

Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Research Abstract Details 

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Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Abstract Text:

Wanke Zhang,Hua Meng,Zhen-Hua Li,Zhenju Shu,Xiuye Ma,Bin-Xian Zhang,

It has been shown that store-operated Ca(2+) influx (SOC) plays critical roles in the activation of endothelial nitric oxide (NO) synthase (eNOS) and generation of NO in endothelial cells. Recent studies indicate stromal interaction molecule 1 (STIM1) is the molecule responsible for SOC activation following Ca(2+) depletion in the ER. Retinoic acids (RA) have beneficial effects in the treatment of renal diseases. The mechanism of the RA action is still largely unknown. In the current study, we used primary cultured rat mesangial cells to examine the effect of RA on SOC and STIM1. In these cells, BK caused concentration-dependent [Ca(2+)](i) mobilization. Treatment of the cells with RA, while it had no effect on the initial peak, reduced the plateau phase of BK-mediated [Ca(2+)](i) response, indicating the inhibition of SOC by RA. The level of STIM1 protein but not mRNA in RA-treated cells was significantly reduced. RA treatment did not affect TGF-beta-mediated gradual Ca(2+) influx which occurred by superoxide anion-mediated mechanism, indicating RA treatment specifically inhibited SOC in mesangial cells. RT-PCR and Western blot analysis demonstrated that eNOS was expressed in rat mesangial cells grown in media containing 11 and 30 but not 5.5 mM glucose. Downregulation of STIM1 protein and BK-induced SOC by RA treatment or STIM1 dsRNA were associated with abolished NO production. The 26S proteasome inhibitor lactacystin blocked the RA-mediated downregulation of BK-induced SOC, suggesting that ubiquitin-proteasome pathway may be involved in RA-mediated STIM1 protein downregulation in rat mesangial cells. Our data suggest that glucose-induced eNOS expression and NO production in mesangial cells may contribute to hyperfiltration in diabetes and RA may exert beneficial effects by downregulation of STIM1 and SOC in mesangial cells.

Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Publishing Authors By Initials

W Zhang,H Meng,ZH Li,Z Shu,X Ma,BX Zhang,

For similar organic chemicals: hydrocarbons: hydrocarbons, acyclic: alkenes: polyenes: carotenoids: retinoids: vitamin a: tretinoin research abstracts see: organic chemicals: hydrocarbons: hydrocarbons, acyclic: alkenes: polyenes: carotenoids: retinoids: vitamin a: tretinoin research

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Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: American journal of physiology. Renal physiology

VOLUME: 292

Page Numbers: F1054-64

Journal Abbreviation: Am. J. Physiol. Renal Physiol.

ISSN: 0363-6127

DAY: 7

MONTH: 11

YEAR: 2006

Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901990

Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Keywords Mesh Terms:

KEYWORDS: Tretinoin

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells. Information

Substance Name: Proteasome Endopeptidase Complex

Registry Number: EC 3.4.25.1

Grant and Affiliation Information for Regulation of STIM1, store-operated Ca2+ influx, and nitric oxide generation by retinoic acid in rat mesangial cells.

AFFILIATION: Geriatric Research, Education, and Clinical Center, South Texas Veterans Health Care System, Audie L. Murphy Division, University of Texas Health Science Center San Antonio, San Antonio, Texas, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01-HL-75011

ACRONYM: HL

MEDLINETA: Am J Physiol Renal Physiol

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