Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells

Background: In response to various stimuli, heat shock protein 27 (Hsp27) functions as an anti-apoptotic or/and anti-inflammatory factor which confers a survival advantage to cells. This study was aimed to explore whether Hsp27 also has a cytoprotective role in human renal tubular epithelial cells,...

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Main Authors: Chunmei Li, Jiang Wu, Yuan Li, Guangqun Xing
Format: Article
Language:English
Published: Cell Physiol Biochem Press GmbH & Co KG 2017-04-01
Series:Cellular Physiology and Biochemistry
Subjects:
Online Access:http://www.karger.com/Article/FullText/475636
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author Chunmei Li
Jiang Wu
Yuan Li
Guangqun Xing
author_facet Chunmei Li
Jiang Wu
Yuan Li
Guangqun Xing
author_sort Chunmei Li
collection DOAJ
description Background: In response to various stimuli, heat shock protein 27 (Hsp27) functions as an anti-apoptotic or/and anti-inflammatory factor which confers a survival advantage to cells. This study was aimed to explore whether Hsp27 also has a cytoprotective role in human renal tubular epithelial cells, and to evaluate its potential in treating septic acute kidney injury (septic AKI). Methods: HK-2 cells were subjected to different concentrations (0-10 µg/mL) of lipopolysaccharide (LPS) for various times (0-24 h) to establish a septic AKI model in vitro. Before LPS administration, HK-2 cells were transfected either with vectors or siRNA against Hsp27, and the changes in cell viability and apoptotic cells rate were assessed using CCK-8 and flow cytometry. The expression changes in apoptosis-related proteins, proinflammatory cytokines and chemokine, as well as main factors in NF-κB and JNK pathways were mainly determined by Western blotting. Besides, the relationship between Hsp27 and Bcl-2 was detected by co-immunoprecipitation. Results: LPS remarkably damaged HK-2 cells by reduction of cell viability, induction of apoptosis, and stimulation of proinflammatory cytokines and chemokine release. Hsp27 overexpression significantly impaired LPS-induced damage in HK-2 cells. Hsp27 overexpression couldn’t alter the mRNA level of Bcl-2, but could interact with Bcl-2 at an endogenous level. Both NF-κB and JNK pathways were activated by LPS, while were blocked in Hsp27-overexpressing cells. Conclusion: Hsp27 overexpression conferred a survival advantage to LPS-injured HK-2 cells by controlling cell viability, apoptosis and inflammation, possibly via interaction with Bcl-2 and modulation of NF-κB and JNK pathways.
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spelling doaj.art-b729dee29d70484e8804c9abf676e9622022-12-22T00:49:18ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782017-04-014162211222010.1159/000475636475636Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 CellsChunmei LiJiang WuYuan LiGuangqun XingBackground: In response to various stimuli, heat shock protein 27 (Hsp27) functions as an anti-apoptotic or/and anti-inflammatory factor which confers a survival advantage to cells. This study was aimed to explore whether Hsp27 also has a cytoprotective role in human renal tubular epithelial cells, and to evaluate its potential in treating septic acute kidney injury (septic AKI). Methods: HK-2 cells were subjected to different concentrations (0-10 µg/mL) of lipopolysaccharide (LPS) for various times (0-24 h) to establish a septic AKI model in vitro. Before LPS administration, HK-2 cells were transfected either with vectors or siRNA against Hsp27, and the changes in cell viability and apoptotic cells rate were assessed using CCK-8 and flow cytometry. The expression changes in apoptosis-related proteins, proinflammatory cytokines and chemokine, as well as main factors in NF-κB and JNK pathways were mainly determined by Western blotting. Besides, the relationship between Hsp27 and Bcl-2 was detected by co-immunoprecipitation. Results: LPS remarkably damaged HK-2 cells by reduction of cell viability, induction of apoptosis, and stimulation of proinflammatory cytokines and chemokine release. Hsp27 overexpression significantly impaired LPS-induced damage in HK-2 cells. Hsp27 overexpression couldn’t alter the mRNA level of Bcl-2, but could interact with Bcl-2 at an endogenous level. Both NF-κB and JNK pathways were activated by LPS, while were blocked in Hsp27-overexpressing cells. Conclusion: Hsp27 overexpression conferred a survival advantage to LPS-injured HK-2 cells by controlling cell viability, apoptosis and inflammation, possibly via interaction with Bcl-2 and modulation of NF-κB and JNK pathways.http://www.karger.com/Article/FullText/475636Heat shock protein 27 (Hsp27)Lipopolysaccharide (LPS)HK-2 cellsSeptic acute kidney injury (septic AKI)Bcl-2NF-κBJNK pathways
spellingShingle Chunmei Li
Jiang Wu
Yuan Li
Guangqun Xing
Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells
Cellular Physiology and Biochemistry
Heat shock protein 27 (Hsp27)
Lipopolysaccharide (LPS)
HK-2 cells
Septic acute kidney injury (septic AKI)
Bcl-2
NF-κB
JNK pathways
title Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells
title_full Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells
title_fullStr Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells
title_full_unstemmed Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells
title_short Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells
title_sort cytoprotective effect of heat shock protein 27 against lipopolysaccharide induced apoptosis of renal epithelial hk 2 cells
topic Heat shock protein 27 (Hsp27)
Lipopolysaccharide (LPS)
HK-2 cells
Septic acute kidney injury (septic AKI)
Bcl-2
NF-κB
JNK pathways
url http://www.karger.com/Article/FullText/475636
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AT jiangwu cytoprotectiveeffectofheatshockprotein27againstlipopolysaccharideinducedapoptosisofrenalepithelialhk2cells
AT yuanli cytoprotectiveeffectofheatshockprotein27againstlipopolysaccharideinducedapoptosisofrenalepithelialhk2cells
AT guangqunxing cytoprotectiveeffectofheatshockprotein27againstlipopolysaccharideinducedapoptosisofrenalepithelialhk2cells