Roles of TGF-β Signaling Pathway in Endoplasmic Reticulum Stress in Endothelial Cells Stimulated with Cigarette Smoke Extract

To investigate the role of signaling pathway in the effect of endoplasmic reticulum stress(ER stress) in endothelial cells stimulated with cigarette smoke extract(CSE). Human umbilical vein endothelial cells(HUVECs) were cultured and divided into 3 groups: CSE-stimulated group, CSE-stimulated with 4...

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Published inCurrent medical science Vol. 37; no. 5; pp. 699 - 704
Main Author 黄宏;丁秋丽;朱慧芬;杨道锋
Format Journal Article
LanguageEnglish
Published Wuhan Huazhong University of Science and Technology 01.10.2017
Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China%Department of Respiratory Medicine, The Central Hospital of Xiaogan, Xiaogan 432000, China%Department of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China%Department of Infectious Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
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Summary:To investigate the role of signaling pathway in the effect of endoplasmic reticulum stress(ER stress) in endothelial cells stimulated with cigarette smoke extract(CSE). Human umbilical vein endothelial cells(HUVECs) were cultured and divided into 3 groups: CSE-stimulated group, CSE-stimulated with 4-PBA group, and negative control group. HUVECs were cultured and stimulated with CSE at concentrations of 5%, 10% and 20%, respectively, mR NA of CXCL-8 and GRP78 was detected by real-time PCR. ELISA was performed to test the expression of CXCL-8 protein, and neutrophils migration was detected by Transwell board test. The NF-κB, ERK, p38 MAPK and transforming growth factor beta(TGF-β) were detected by flow cytometry. The mRNA of CXCL-8 and GRP78 increased in CSE-stimulated HUVECs(P〈0.05). Furthermore, it was concentration-dependent. 4-PBA significantly reduced the expression of CXCL-8 protein(P〈0.05) and neutrophil migration(P〈0.05). The TGF-β, rather than the NF-κB, ERK and P38 MAPK pathway might be involved in ER stress stimulated by CSE. CSE induced neutrophils migration by increasing the expression of CXCL-8 in endothelial cells. ER stress might play a role in the effect of neutrophils migration stimulated with CSE, and TGF-β pathway may contribute to the ER stress in HUVECs.
Bibliography:endoplasmic reticulum stress; cigarette smoke extract; endothelial cells; neutrophil migration; signaling pathway
42-1679/R
To investigate the role of signaling pathway in the effect of endoplasmic reticulum stress(ER stress) in endothelial cells stimulated with cigarette smoke extract(CSE). Human umbilical vein endothelial cells(HUVECs) were cultured and divided into 3 groups: CSE-stimulated group, CSE-stimulated with 4-PBA group, and negative control group. HUVECs were cultured and stimulated with CSE at concentrations of 5%, 10% and 20%, respectively, mR NA of CXCL-8 and GRP78 was detected by real-time PCR. ELISA was performed to test the expression of CXCL-8 protein, and neutrophils migration was detected by Transwell board test. The NF-κB, ERK, p38 MAPK and transforming growth factor beta(TGF-β) were detected by flow cytometry. The mRNA of CXCL-8 and GRP78 increased in CSE-stimulated HUVECs(P〈0.05). Furthermore, it was concentration-dependent. 4-PBA significantly reduced the expression of CXCL-8 protein(P〈0.05) and neutrophil migration(P〈0.05). The TGF-β, rather than the NF-κB, ERK and P38 MAPK pathway might be involved in ER stress stimulated by CSE. CSE induced neutrophils migration by increasing the expression of CXCL-8 in endothelial cells. ER stress might play a role in the effect of neutrophils migration stimulated with CSE, and TGF-β pathway may contribute to the ER stress in HUVECs.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1672-0733
2096-5230
1993-1352
1993-1352
2523-899X
DOI:10.1007/s11596-017-1791-z