Epoxyeicosatrienoic acids attenuating hypotonic-induced apoptosis of IMCD cells via γ-ENaC inhibition

Luyun Wang, Yang Liu, Huamin Wang, Xun Liu, Jie Chen, Mong-Heng Wang, Jingfeng Wang, Hui Huang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Inner medulla collecting duct (IMCD) cells are the key part for urinary concentration. Hypotonic stress may trigger apoptosis of IMCD cells and induce renal injury. Epoxyeicosatrienoic acids (EETs) play an important role in anti-apoptosis, but their roles in hypotonic-induced apoptosis of IMCD cells are still unclear. Here we found increasing exogenous 11, 12-EET or endogenous EETs with Ad-CMV-CYP2C23-EGFP transfection decreased apoptosis of IMCD cells induced by hypotonic stress. Moreover, up-regulation of γ-ENaC induced by hypotonic stress was abolished by elevation of exogenous or endogenous EETs. Collectively, this study illustrated that EETs attenuated hypotonic-induced apoptosis of IMCD cells, and that regulation of γ-ENAC may be a possible mechanism contributing to the anti-apoptotic effect of EETs in response to hypotonic stress.

Original languageEnglish (US)
Article numbere94400
JournalPloS one
Volume9
Issue number4
DOIs
StatePublished - Apr 8 2014

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Ducts
Osmotic Pressure
apoptosis
Apoptosis
Acids
acids
cells
transfection
Transfection
stress response
Up-Regulation
kidneys
Kidney
Wounds and Injuries

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

Epoxyeicosatrienoic acids attenuating hypotonic-induced apoptosis of IMCD cells via γ-ENaC inhibition. / Wang, Luyun; Liu, Yang; Wang, Huamin; Liu, Xun; Chen, Jie; Wang, Mong-Heng; Wang, Jingfeng; Huang, Hui.

In: PloS one, Vol. 9, No. 4, e94400, 08.04.2014.

Research output: Contribution to journalArticle

Wang, Luyun ; Liu, Yang ; Wang, Huamin ; Liu, Xun ; Chen, Jie ; Wang, Mong-Heng ; Wang, Jingfeng ; Huang, Hui. / Epoxyeicosatrienoic acids attenuating hypotonic-induced apoptosis of IMCD cells via γ-ENaC inhibition. In: PloS one. 2014 ; Vol. 9, No. 4.
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