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Simvastatin increases Prolyl-4-Hydroxylase [alpha]1 expression in atherosclerotic plaque and ox-LDL-stimulated human aortic smooth muscle cells via p38 MAPK and ERK1/2 signaling

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.yjmcc.2013.09.010 Byline: Kai Zhang, Xiao Meng, Jing Kong, Fang-Fang Liu, Jian-Min Yang, Fei Gao, Yun Zhang, Cheng Zhang Abstract: Prolyl-4-Hydroxylase [alpha]1 (P4H[alpha]1) is essential for collagen synthesi... Full description

Journal Title: Journal of Molecular and Cellular Cardiology Dec, 2013, Vol.65, p.43(8)
Main Author: Zhang, Kai
Other Authors: Meng, Xiao , Kong, Jing , Liu, Fang - Fang , Yang, Jian - Min , Gao, Fei , Zhang, Yun , Zhang, Cheng
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Cengage Learning, Inc.
ID: ISSN: 0022-2828
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recordid: gale_ofa351828263
title: Simvastatin increases Prolyl-4-Hydroxylase [alpha]1 expression in atherosclerotic plaque and ox-LDL-stimulated human aortic smooth muscle cells via p38 MAPK and ERK1/2 signaling
format: Article
creator:
  • Zhang, Kai
  • Meng, Xiao
  • Kong, Jing
  • Liu, Fang - Fang
  • Yang, Jian - Min
  • Gao, Fei
  • Zhang, Yun
  • Zhang, Cheng
subjects:
  • Collagen
  • Low Density Lipoproteins
  • Smooth Muscle
  • Simvastatin
  • Antilipemic Agents
ispartof: Journal of Molecular and Cellular Cardiology, Dec, 2013, Vol.65, p.43(8)
description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.yjmcc.2013.09.010 Byline: Kai Zhang, Xiao Meng, Jing Kong, Fang-Fang Liu, Jian-Min Yang, Fei Gao, Yun Zhang, Cheng Zhang Abstract: Prolyl-4-Hydroxylase [alpha]1 (P4H[alpha]1) is essential for collagen synthesis but the effect of statin on P4H[alpha]1 is unknown. We hypothesize that simvastatin may increase the expression of P4H[alpha]1 in atherosclerotic plaques and ox-LDL-stimulated human aortic smooth muscle cells (HASMCs). In HASMCs, ox-LDL suppressed P4H[alpha]1 expression significantly with peak value occurring at 50ug/ml treated for 8h. Ox-LDL also inhibited the expression of type I and III collagen and increased the phosphorylation level of p38 MAPK and ERK1/2, but blockade or silencing of p38 and ERK1/2 inhibited the suppressive effect of ox-LDL on P4H[alpha]1. Then HASMCs were stimulated with or without ox-LDL (50ug/ml) for 8h after simvastatin pretreatment for 1h. Simvastatin significantly attenuated the suppressive effect of ox-LDL on P4H[alpha]1 and collagen production by inhibiting ox-LDL uptake and the activation of p38 MAPK and ERK1/2. In apolipoprotein E-deficient mice, simvastatin and the inhibitors of p38 and ERK1/2 significantly increased the stability of the carotid plaques. We also found that simvastatin significantly increased the expression of P4H[alpha]1 and collagen possibly due to decreased ox-LDL content and phosphorylation of p38 and ERK1/2 in plaques. Thus, simvastatin increases P4H[alpha]1 and collagen expression in ox-LDL-stimulated HASMCs and atherosclerotic plaques via p38 MAPK and ERK1/2, thereby exerting a plaque stabilizing effect. Article History: Received 8 May 2013; Revised 29 August 2013; Accepted 20 September 2013
language: English
source: Cengage Learning, Inc.
identifier: ISSN: 0022-2828
fulltext: fulltext
issn:
  • 0022-2828
  • 00222828
url: Link


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titleSimvastatin increases Prolyl-4-Hydroxylase [alpha]1 expression in atherosclerotic plaque and ox-LDL-stimulated human aortic smooth muscle cells via p38 MAPK and ERK1/2 signaling
creatorZhang, Kai ; Meng, Xiao ; Kong, Jing ; Liu, Fang - Fang ; Yang, Jian - Min ; Gao, Fei ; Zhang, Yun ; Zhang, Cheng
ispartofJournal of Molecular and Cellular Cardiology, Dec, 2013, Vol.65, p.43(8)
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subjectCollagen ; Low Density Lipoproteins ; Smooth Muscle ; Simvastatin ; Antilipemic Agents
descriptionTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.yjmcc.2013.09.010 Byline: Kai Zhang, Xiao Meng, Jing Kong, Fang-Fang Liu, Jian-Min Yang, Fei Gao, Yun Zhang, Cheng Zhang Abstract: Prolyl-4-Hydroxylase [alpha]1 (P4H[alpha]1) is essential for collagen synthesis but the effect of statin on P4H[alpha]1 is unknown. We hypothesize that simvastatin may increase the expression of P4H[alpha]1 in atherosclerotic plaques and ox-LDL-stimulated human aortic smooth muscle cells (HASMCs). In HASMCs, ox-LDL suppressed P4H[alpha]1 expression significantly with peak value occurring at 50ug/ml treated for 8h. Ox-LDL also inhibited the expression of type I and III collagen and increased the phosphorylation level of p38 MAPK and ERK1/2, but blockade or silencing of p38 and ERK1/2 inhibited the suppressive effect of ox-LDL on P4H[alpha]1. Then HASMCs were stimulated with or without ox-LDL (50ug/ml) for 8h after simvastatin pretreatment for 1h. Simvastatin significantly attenuated the suppressive effect of ox-LDL on P4H[alpha]1 and collagen production by inhibiting ox-LDL uptake and the activation of p38 MAPK and ERK1/2. In apolipoprotein E-deficient mice, simvastatin and the inhibitors of p38 and ERK1/2 significantly increased the stability of the carotid plaques. We also found that simvastatin significantly increased the expression of P4H[alpha]1 and collagen possibly due to decreased ox-LDL content and phosphorylation of p38 and ERK1/2 in plaques. Thus, simvastatin increases P4H[alpha]1 and collagen expression in ox-LDL-stimulated HASMCs and atherosclerotic plaques via p38 MAPK and ERK1/2, thereby exerting a plaque stabilizing effect. Article History: Received 8 May 2013; Revised 29 August 2013; Accepted 20 September 2013
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titleSimvastatin increases Prolyl-4-Hydroxylase [alpha]1 expression in atherosclerotic plaque and ox-LDL-stimulated human aortic smooth muscle cells via p38 MAPK and ERK1/2 signaling.
descriptionTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.yjmcc.2013.09.010 Byline: Kai Zhang, Xiao Meng, Jing Kong, Fang-Fang Liu, Jian-Min Yang, Fei Gao, Yun Zhang, Cheng Zhang Abstract: Prolyl-4-Hydroxylase [alpha]1 (P4H[alpha]1) is essential for collagen synthesis but the effect of statin on P4H[alpha]1 is unknown. We hypothesize that simvastatin may increase the expression of P4H[alpha]1 in atherosclerotic plaques and ox-LDL-stimulated human aortic smooth muscle cells (HASMCs). In HASMCs, ox-LDL suppressed P4H[alpha]1 expression significantly with peak value occurring at 50ug/ml treated for 8h. Ox-LDL also inhibited the expression of type I and III collagen and increased the phosphorylation level of p38 MAPK and ERK1/2, but blockade or silencing of p38 and ERK1/2 inhibited the suppressive effect of ox-LDL on P4H[alpha]1. Then HASMCs were stimulated with or without ox-LDL (50ug/ml) for 8h after simvastatin pretreatment for 1h. Simvastatin significantly attenuated the suppressive effect of ox-LDL on P4H[alpha]1 and collagen production by inhibiting ox-LDL uptake and the activation of p38 MAPK and ERK1/2. In apolipoprotein E-deficient mice, simvastatin and the inhibitors of p38 and ERK1/2 significantly increased the stability of the carotid plaques. We also found that simvastatin significantly increased the expression of P4H[alpha]1 and collagen possibly due to decreased ox-LDL content and phosphorylation of p38 and ERK1/2 in plaques. Thus, simvastatin increases P4H[alpha]1 and collagen expression in ox-LDL-stimulated HASMCs and atherosclerotic plaques via p38 MAPK and ERK1/2, thereby exerting a plaque stabilizing effect. Article History: Received 8 May 2013; Revised 29 August 2013; Accepted 20 September 2013
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abstractTo link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.yjmcc.2013.09.010 Byline: Kai Zhang, Xiao Meng, Jing Kong, Fang-Fang Liu, Jian-Min Yang, Fei Gao, Yun Zhang, Cheng Zhang Abstract: Prolyl-4-Hydroxylase [alpha]1 (P4H[alpha]1) is essential for collagen synthesis but the effect of statin on P4H[alpha]1 is unknown. We hypothesize that simvastatin may increase the expression of P4H[alpha]1 in atherosclerotic plaques and ox-LDL-stimulated human aortic smooth muscle cells (HASMCs). In HASMCs, ox-LDL suppressed P4H[alpha]1 expression significantly with peak value occurring at 50ug/ml treated for 8h. Ox-LDL also inhibited the expression of type I and III collagen and increased the phosphorylation level of p38 MAPK and ERK1/2, but blockade or silencing of p38 and ERK1/2 inhibited the suppressive effect of ox-LDL on P4H[alpha]1. Then HASMCs were stimulated with or without ox-LDL (50ug/ml) for 8h after simvastatin pretreatment for 1h. Simvastatin significantly attenuated the suppressive effect of ox-LDL on P4H[alpha]1 and collagen production by inhibiting ox-LDL uptake and the activation of p38 MAPK and ERK1/2. In apolipoprotein E-deficient mice, simvastatin and the inhibitors of p38 and ERK1/2 significantly increased the stability of the carotid plaques. We also found that simvastatin significantly increased the expression of P4H[alpha]1 and collagen possibly due to decreased ox-LDL content and phosphorylation of p38 and ERK1/2 in plaques. Thus, simvastatin increases P4H[alpha]1 and collagen expression in ox-LDL-stimulated HASMCs and atherosclerotic plaques via p38 MAPK and ERK1/2, thereby exerting a plaque stabilizing effect. Article History: Received 8 May 2013; Revised 29 August 2013; Accepted 20 September 2013
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