Hypothermia may attenuate ischemia/reperfusion-induced cardiomyocyte death by reducing autophagy

Bor Chih Cheng, Huei Sheng Huang, Chien Ming Chao, Chuan Chih Hsu, Chia Ying Chen, Ching Ping Chang

研究成果: 雜誌貢獻文章

18 引文 (Scopus)

摘要

Objective We sought to assess the effect of therapeutic hypothermia on the autophagy that occurred in ischemia-reperfused (IR) H9c2 cardiomyocytes. Methods In control studies, the H9c2 cells at a density of 1 × 105 per culture dish in six-well plate were exposed to normoxic culture medium at 37 C for 12 h. All assays contained appropriate controls and were performed in triplicate and repeated on three separately initiated cultures. In hypothermia-treated group, the ischemic and hypoxic cells were maintained in a 32 C incubation. The trypan blue exclusion method was used to assess the cell viability. Autophagy was evaluated by determining both the microtubule- associated protein 1 light chain 3 [LC3] levels and punctuate distribution of the autophagic vesicle associated form [LC3-II]. Results The results were mean ± standard error of mean of triplicates. The viable cell percentage for control group, IR group, and IR group treated with hypothermia at the start of ischemia, or reperfusion were 100% ± 9%, 20% ± 1%, 32% ± 3%, and 41% ± 3%, respectively. The cell death in I/R H9c2 cells was positively associated with increased LC3 levels and punctuate distribution of (LC3-II). Mild hypothermia adopted at the start of ischemia or reperfusion significantly reduced both the cell death and the autophagy in H9c2 cells. Conclusion Our data indicate that in H9c2, IR stimulates cell autophagy and causes cell death, which can be attenuated by mild hypothermia. Our results, if further confirmed in vivo, may have important clinical implications during IR injury.

原文英語
頁(從 - 到)2064-2069
頁數6
期刊International Journal of Cardiology
168
發行號3
DOIs
出版狀態已發佈 - 十月 3 2013

指紋

Autophagy
Hypothermia
Cardiac Myocytes
Reperfusion
Ischemia
Light
Cell Death
Induced Hypothermia
Microtubule-Associated Proteins
Trypan Blue
Culture Media
Cause of Death
Cell Survival
Control Groups
Wounds and Injuries

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

引用此文

Hypothermia may attenuate ischemia/reperfusion-induced cardiomyocyte death by reducing autophagy. / Cheng, Bor Chih; Huang, Huei Sheng; Chao, Chien Ming; Hsu, Chuan Chih; Chen, Chia Ying; Chang, Ching Ping.

於: International Journal of Cardiology, 卷 168, 編號 3, 03.10.2013, p. 2064-2069.

研究成果: 雜誌貢獻文章

Cheng, Bor Chih ; Huang, Huei Sheng ; Chao, Chien Ming ; Hsu, Chuan Chih ; Chen, Chia Ying ; Chang, Ching Ping. / Hypothermia may attenuate ischemia/reperfusion-induced cardiomyocyte death by reducing autophagy. 於: International Journal of Cardiology. 2013 ; 卷 168, 編號 3. 頁 2064-2069.
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abstract = "Objective We sought to assess the effect of therapeutic hypothermia on the autophagy that occurred in ischemia-reperfused (IR) H9c2 cardiomyocytes. Methods In control studies, the H9c2 cells at a density of 1 × 105 per culture dish in six-well plate were exposed to normoxic culture medium at 37 C for 12 h. All assays contained appropriate controls and were performed in triplicate and repeated on three separately initiated cultures. In hypothermia-treated group, the ischemic and hypoxic cells were maintained in a 32 C incubation. The trypan blue exclusion method was used to assess the cell viability. Autophagy was evaluated by determining both the microtubule- associated protein 1 light chain 3 [LC3] levels and punctuate distribution of the autophagic vesicle associated form [LC3-II]. Results The results were mean ± standard error of mean of triplicates. The viable cell percentage for control group, IR group, and IR group treated with hypothermia at the start of ischemia, or reperfusion were 100{\%} ± 9{\%}, 20{\%} ± 1{\%}, 32{\%} ± 3{\%}, and 41{\%} ± 3{\%}, respectively. The cell death in I/R H9c2 cells was positively associated with increased LC3 levels and punctuate distribution of (LC3-II). Mild hypothermia adopted at the start of ischemia or reperfusion significantly reduced both the cell death and the autophagy in H9c2 cells. Conclusion Our data indicate that in H9c2, IR stimulates cell autophagy and causes cell death, which can be attenuated by mild hypothermia. Our results, if further confirmed in vivo, may have important clinical implications during IR injury.",
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AU - Chao, Chien Ming

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N2 - Objective We sought to assess the effect of therapeutic hypothermia on the autophagy that occurred in ischemia-reperfused (IR) H9c2 cardiomyocytes. Methods In control studies, the H9c2 cells at a density of 1 × 105 per culture dish in six-well plate were exposed to normoxic culture medium at 37 C for 12 h. All assays contained appropriate controls and were performed in triplicate and repeated on three separately initiated cultures. In hypothermia-treated group, the ischemic and hypoxic cells were maintained in a 32 C incubation. The trypan blue exclusion method was used to assess the cell viability. Autophagy was evaluated by determining both the microtubule- associated protein 1 light chain 3 [LC3] levels and punctuate distribution of the autophagic vesicle associated form [LC3-II]. Results The results were mean ± standard error of mean of triplicates. The viable cell percentage for control group, IR group, and IR group treated with hypothermia at the start of ischemia, or reperfusion were 100% ± 9%, 20% ± 1%, 32% ± 3%, and 41% ± 3%, respectively. The cell death in I/R H9c2 cells was positively associated with increased LC3 levels and punctuate distribution of (LC3-II). Mild hypothermia adopted at the start of ischemia or reperfusion significantly reduced both the cell death and the autophagy in H9c2 cells. Conclusion Our data indicate that in H9c2, IR stimulates cell autophagy and causes cell death, which can be attenuated by mild hypothermia. Our results, if further confirmed in vivo, may have important clinical implications during IR injury.

AB - Objective We sought to assess the effect of therapeutic hypothermia on the autophagy that occurred in ischemia-reperfused (IR) H9c2 cardiomyocytes. Methods In control studies, the H9c2 cells at a density of 1 × 105 per culture dish in six-well plate were exposed to normoxic culture medium at 37 C for 12 h. All assays contained appropriate controls and were performed in triplicate and repeated on three separately initiated cultures. In hypothermia-treated group, the ischemic and hypoxic cells were maintained in a 32 C incubation. The trypan blue exclusion method was used to assess the cell viability. Autophagy was evaluated by determining both the microtubule- associated protein 1 light chain 3 [LC3] levels and punctuate distribution of the autophagic vesicle associated form [LC3-II]. Results The results were mean ± standard error of mean of triplicates. The viable cell percentage for control group, IR group, and IR group treated with hypothermia at the start of ischemia, or reperfusion were 100% ± 9%, 20% ± 1%, 32% ± 3%, and 41% ± 3%, respectively. The cell death in I/R H9c2 cells was positively associated with increased LC3 levels and punctuate distribution of (LC3-II). Mild hypothermia adopted at the start of ischemia or reperfusion significantly reduced both the cell death and the autophagy in H9c2 cells. Conclusion Our data indicate that in H9c2, IR stimulates cell autophagy and causes cell death, which can be attenuated by mild hypothermia. Our results, if further confirmed in vivo, may have important clinical implications during IR injury.

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