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Inhibition of ROS-activated ERK1/2 pathway contributes to the protection of H 2 S against chemical hypoxia-induced injury in H9c2 cells

Hydrogen sulfide (H 2 S) has been shown to exert cardioprotective effects. However, the roles of extracellular signal-regulated protein kinases 1/2 (ERK1/2) in H 2 S-induced cardioprotection have not been completely elucidated. In this study, cobalt chloride (CoCl 2 ), a chemical hypoxia mimetic age... Full description

Journal Title: Molecular and Cellular Biochemistry 2012, Vol.362(1), pp.149-157
Main Author: Dong, Xiao-Bian
Other Authors: Yang, Chun-Tao , Zheng, Dong-Dan , Mo, Li-Qiu , Wang, Xiu-Yu , Lan, Ai-Ping , Hu, Fen , Chen, Pei-Xi , Feng, Jian-Qiang , Zhang, Mei-Fen , Liao, Xin-Xue
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0300-8177 ; E-ISSN: 1573-4919 ; DOI: 10.1007/s11010-011-1137-2
Link: http://dx.doi.org/10.1007/s11010-011-1137-2
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recordid: springer_jour10.1007/s11010-011-1137-2
title: Inhibition of ROS-activated ERK1/2 pathway contributes to the protection of H 2 S against chemical hypoxia-induced injury in H9c2 cells
format: Article
creator:
  • Dong, Xiao-Bian
  • Yang, Chun-Tao
  • Zheng, Dong-Dan
  • Mo, Li-Qiu
  • Wang, Xiu-Yu
  • Lan, Ai-Ping
  • Hu, Fen
  • Chen, Pei-Xi
  • Feng, Jian-Qiang
  • Zhang, Mei-Fen
  • Liao, Xin-Xue
subjects:
  • Hydrogen sulfide
  • Extracellular signal-regulated protein kinases 1/2
  • Cardioprotection
  • Chemical hypoxia
  • H9c2 cells
ispartof: Molecular and Cellular Biochemistry, 2012, Vol.362(1), pp.149-157
description: Hydrogen sulfide (H 2 S) has been shown to exert cardioprotective effects. However, the roles of extracellular signal-regulated protein kinases 1/2 (ERK1/2) in H 2 S-induced cardioprotection have not been completely elucidated. In this study, cobalt chloride (CoCl 2 ), a chemical hypoxia mimetic agent, was applied to treat H9c2 cells to establish a chemical hypoxia-induced cardiomyocyte injury model. The results showed that pretreatment with NaHS (a donor of H 2 S) before exposure to CoCl 2 attenuated the decreased cell viability, the increased apoptosis rate, the loss of mitochondrial membrane potential (ΔΨm), and the intracellular accumulation of reactive oxygen species (ROS) in H9c2 cells. Exposure of H9c2 cells to CoCl 2 or hydrogen peroxide (H 2 O 2 ) upregulated expression of phosphorylated (p) ERK1/2, which was reduced by pretreatment with NaHS or N -acetyl- l -cysteine, a ROS scavenger. More importantly, U0126, a selective inhibitor of ERK1/2, mimicked the above cytoprotection of H 2 S against CoCl 2 -induced injury in H9c2 cells. In conclusion, these results indicate that H 2 S protects H9c2 cells against chemical hypoxia-induced injury partially by inhibiting ROS-mediated activation of ERK1/2.
language: eng
source:
identifier: ISSN: 0300-8177 ; E-ISSN: 1573-4919 ; DOI: 10.1007/s11010-011-1137-2
fulltext: fulltext
issn:
  • 1573-4919
  • 15734919
  • 0300-8177
  • 03008177
url: Link


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titleInhibition of ROS-activated ERK1/2 pathway contributes to the protection of H 2 S against chemical hypoxia-induced injury in H9c2 cells
creatorDong, Xiao-Bian ; Yang, Chun-Tao ; Zheng, Dong-Dan ; Mo, Li-Qiu ; Wang, Xiu-Yu ; Lan, Ai-Ping ; Hu, Fen ; Chen, Pei-Xi ; Feng, Jian-Qiang ; Zhang, Mei-Fen ; Liao, Xin-Xue
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subjectHydrogen sulfide ; Extracellular signal-regulated protein kinases 1/2 ; Cardioprotection ; Chemical hypoxia ; H9c2 cells
descriptionHydrogen sulfide (H 2 S) has been shown to exert cardioprotective effects. However, the roles of extracellular signal-regulated protein kinases 1/2 (ERK1/2) in H 2 S-induced cardioprotection have not been completely elucidated. In this study, cobalt chloride (CoCl 2 ), a chemical hypoxia mimetic agent, was applied to treat H9c2 cells to establish a chemical hypoxia-induced cardiomyocyte injury model. The results showed that pretreatment with NaHS (a donor of H 2 S) before exposure to CoCl 2 attenuated the decreased cell viability, the increased apoptosis rate, the loss of mitochondrial membrane potential (ΔΨm), and the intracellular accumulation of reactive oxygen species (ROS) in H9c2 cells. Exposure of H9c2 cells to CoCl 2 or hydrogen peroxide (H 2 O 2 ) upregulated expression of phosphorylated (p) ERK1/2, which was reduced by pretreatment with NaHS or N -acetyl- l -cysteine, a ROS scavenger. More importantly, U0126, a selective inhibitor of ERK1/2, mimicked the above cytoprotection of H 2 S against CoCl 2 -induced injury in H9c2 cells. In conclusion, these results indicate that H 2 S protects H9c2 cells against chemical hypoxia-induced injury partially by inhibiting ROS-mediated activation of ERK1/2.
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titleInhibition of ROS-activated ERK1/2 pathway contributes to the protection of H 2 S against chemical hypoxia-induced injury in H9c2 cells
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abstractHydrogen sulfide (H 2 S) has been shown to exert cardioprotective effects. However, the roles of extracellular signal-regulated protein kinases 1/2 (ERK1/2) in H 2 S-induced cardioprotection have not been completely elucidated. In this study, cobalt chloride (CoCl 2 ), a chemical hypoxia mimetic agent, was applied to treat H9c2 cells to establish a chemical hypoxia-induced cardiomyocyte injury model. The results showed that pretreatment with NaHS (a donor of H 2 S) before exposure to CoCl 2 attenuated the decreased cell viability, the increased apoptosis rate, the loss of mitochondrial membrane potential (ΔΨm), and the intracellular accumulation of reactive oxygen species (ROS) in H9c2 cells. Exposure of H9c2 cells to CoCl 2 or hydrogen peroxide (H 2 O 2 ) upregulated expression of phosphorylated (p) ERK1/2, which was reduced by pretreatment with NaHS or N -acetyl- l -cysteine, a ROS scavenger. More importantly, U0126, a selective inhibitor of ERK1/2, mimicked the above cytoprotection of H 2 S against CoCl 2 -induced injury in H9c2 cells. In conclusion, these results indicate that H 2 S protects H9c2 cells against chemical hypoxia-induced injury partially by inhibiting ROS-mediated activation of ERK1/2.
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