계명대학교 의학도서관 Repository

C/EBP homologous protein (CHOP) gene deficiency attenuates renal ischemia/reperfusion injury in mice.

Metadata Downloads
Author(s)
김지인
Alternative Author(s)
Kim, Jee In
Publication Year
2015
Keyword
C/EBP homologous proteinCHOPER stressIschemiaApoptosis
Abstract
C/EBP homologous protein (CHOP), a transcription factor for the expression of apoptosis-related genes, plays an
important role in endoplasmic reticulum (ER) stress-related organ diseases, including diseases of the kidney.
Here, we investigated the role of CHOP in ischemia/reperfusion (I/R)-induced acute kidney injury using
CHOP-knockout (CHOP−/−) and wild type (CHOP+/+) mice. Fifteen or thirtyminutes of bilateral renal ischemia
(I/R) insult resulted in necrotic and apoptotic tubular epithelial cell death, together with increases in plasma
creatinine (PCr) and blood urea nitrogen (BUN) concentrations. After I/R, BiP/GRP78 and CHOP expressions in
the kidney gradually increased over time. CHOP expression was greater in the outer medulla than that in the
cortex and localized intensely in the nucleus. I/R caused apoptosis of tubular epithelial cells in both CHOP−/−
and CHOP+/+ mice. The number of apoptotic cells after I/R was lower in CHOP−/− mice than that in CHOP+/+
mice. Consistent with the degree of apoptosis, I/R-induced kidney morphological and functional damages were
milder in CHOP−/− than that in CHOP+/+ mice. The cleavage of procaspase-3 and the induction of Bax protein
after I/R were lower in CHOP−/− than that in CHOP+/+ mice. In contrast, the expression levels of Bcl-2, Bcl-xL,
cIAP2, Mcl-1, and XIAP were higher in CHOP−/− than that in CHOP+/+ mice. These results indicate that I/R
induces ER stress, leading to the activation of CHOP-associated apoptosis signals, resulting in renal functional
and histological damages.
Department
Dept. of Molecular Medicine (분자의학)
Publisher
School of Medicine
Citation
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1852(9) : 1895-1901, 2015
Type
Article
ISSN
0925-4439
DOI
10.1016/j.bbadis.2015.06.004
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/32904
Authorize & License
  • AuthorizeOpen
  • EmbargoForever
Files in This Item:

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.