CCN1/CYR61 overexpression in hepatic stellate cells induces ER stress-related apoptosis
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- 作者：Erawan Borkham-Kamphorsta ; ekamphorst@ukaachen.de" class="auth_mail" title="E-mail the corresponding author ; Bettina T. Steffena ; Eddy Van de Leura ; Ute Haasa ; Lidia Tihaaa ; Scott L. Friedmanb ; Ralf Weiskirchena ; rweiskirchen@ukaachen.de" class="auth_mail" title="E-mail the corresponding author
- 关键词：Ad5-CCN1 ; Ad5-CMV-CCN1 ; Ad5-Luc ; Ad5-CMV-Luc ; ATF6 ; activating transcription factor 6 ; β-Gal ; β-galactosidase ; ECM ; extracellular matrix ; ER ; endoplasmic reticulum ; ERAD ; ER-associated protein degradation ; HSC ; hepatic stellate cell(s) ; IRE1 ; inositol-requiring enzyme 1 ; LCN2 ; Lipocalin 2 ; MFB ; myofibroblast(s) ; PC ; hepatocyte(s) ; PERK ; protein kinase R (PKR)-like endoplasmic reticulum kinase ; pMF ; portal myofibroblast(s) ; TUDCA ; tauroursodeoxycholic acid ; TUNEL ; terminal transferase dUTP nick e
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：28
- 期：1
- 页码：34-42
- 全文大小：1930 K
文摘
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High intracellular concentrations of CCN1/CYR61 induce ER stress in HSC.
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10">CCN1/CYR61-induced ER stress results in compensatory unfolded protein response.
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15">When CCN1/CYR61 overload is too high the NF-κB pathway is activated.
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The NF-κB pathway initiates apoptosis in HSC.
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The content of intracellular CCN1/CYR61 is a key switch in limiting hepatic fibrosis.