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Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo
One of the pathological functions of heat shock protein 22 (HSP22) is the association with inflammatory diseases and atherosclerosis. However, the effects of a high-fat diet (HFD) or oxidized low-density lipoprotein (ox-LDL) combined with atorvastatin (ATV) on HSP22 expression are entirely unknown....
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6317682/ https://www.ncbi.nlm.nih.gov/pubmed/30535427 http://dx.doi.org/10.3892/ijmm.2018.4015 |
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author | Chen, Qi Xiang, Jian Gong, Ren Fang, Hai-Yang Xu, Cong-Cong Zhang, Hong-Zhou Wu, Yan-Qing |
author_facet | Chen, Qi Xiang, Jian Gong, Ren Fang, Hai-Yang Xu, Cong-Cong Zhang, Hong-Zhou Wu, Yan-Qing |
author_sort | Chen, Qi |
collection | PubMed |
description | One of the pathological functions of heat shock protein 22 (HSP22) is the association with inflammatory diseases and atherosclerosis. However, the effects of a high-fat diet (HFD) or oxidized low-density lipoprotein (ox-LDL) combined with atorvastatin (ATV) on HSP22 expression are entirely unknown. The present study investigated the effects of ATV on HSP22 expression in HFD-induced atherosclerotic apolipoprotein E-deficient (ApoE(−/−)) mice and in ox-LDL-induced human umbilical vein endothelial cells (HUVECs). Furthermore, the influence of HSP22-knockdown on the HFD- or ox-LDL-induced atherosclerotic model was also examined. It was found that HFD or ox-LDL treatment significantly increased HSP22 expression in the serum and aorta, accompanied by decreased phosphorylated (p)-endothelial nitric oxide synthase (p-eNOS) activity and activated p38 mitogen-activated protein kinase (MAPK). However, these effects were suppressed by treatment with ATV. Furthermore, HSP22-knockdown showed reduced ox-LDL-induced lesions, evidenced by increased p-eNOS activity and inactivated p38 MAPK, while suppression of cell proliferation inhibition and cell cycle arrest were also observed. Taken together, the results of this study suggest that HFD or ox-LDL increased the expression of HSP22 and p-p38 MAPK, and decreased the p-eNOS activity in vitro and in vivo, and ATV could reduce the effects by downregulating HSP22 expression. |
format | Online Article Text |
id | pubmed-6317682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-63176822019-01-24 Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo Chen, Qi Xiang, Jian Gong, Ren Fang, Hai-Yang Xu, Cong-Cong Zhang, Hong-Zhou Wu, Yan-Qing Int J Mol Med Articles One of the pathological functions of heat shock protein 22 (HSP22) is the association with inflammatory diseases and atherosclerosis. However, the effects of a high-fat diet (HFD) or oxidized low-density lipoprotein (ox-LDL) combined with atorvastatin (ATV) on HSP22 expression are entirely unknown. The present study investigated the effects of ATV on HSP22 expression in HFD-induced atherosclerotic apolipoprotein E-deficient (ApoE(−/−)) mice and in ox-LDL-induced human umbilical vein endothelial cells (HUVECs). Furthermore, the influence of HSP22-knockdown on the HFD- or ox-LDL-induced atherosclerotic model was also examined. It was found that HFD or ox-LDL treatment significantly increased HSP22 expression in the serum and aorta, accompanied by decreased phosphorylated (p)-endothelial nitric oxide synthase (p-eNOS) activity and activated p38 mitogen-activated protein kinase (MAPK). However, these effects were suppressed by treatment with ATV. Furthermore, HSP22-knockdown showed reduced ox-LDL-induced lesions, evidenced by increased p-eNOS activity and inactivated p38 MAPK, while suppression of cell proliferation inhibition and cell cycle arrest were also observed. Taken together, the results of this study suggest that HFD or ox-LDL increased the expression of HSP22 and p-p38 MAPK, and decreased the p-eNOS activity in vitro and in vivo, and ATV could reduce the effects by downregulating HSP22 expression. D.A. Spandidos 2019-02 2018-12-03 /pmc/articles/PMC6317682/ /pubmed/30535427 http://dx.doi.org/10.3892/ijmm.2018.4015 Text en Copyright: © Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Chen, Qi Xiang, Jian Gong, Ren Fang, Hai-Yang Xu, Cong-Cong Zhang, Hong-Zhou Wu, Yan-Qing Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo |
title | Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo |
title_full | Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo |
title_fullStr | Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo |
title_full_unstemmed | Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo |
title_short | Atorvastatin downregulates HSP22 expression in an atherosclerotic model in vitro and in vivo |
title_sort | atorvastatin downregulates hsp22 expression in an atherosclerotic model in vitro and in vivo |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6317682/ https://www.ncbi.nlm.nih.gov/pubmed/30535427 http://dx.doi.org/10.3892/ijmm.2018.4015 |
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