Cathepsin B is involved in the heat shock induced cardiomyocytes apoptosis as well as the anti-apoptosis effect of HSP-70

Shu Fen Hsu, Chuan Chih Hsu, Bor Chih Cheng, Cheng Hsien Lin

研究成果: 雜誌貢獻 › 文章

11 引文 (Scopus)

摘要

Cathepsin B is one of the major lysosomal cysteine proteases that plays an important role in apoptosis. Herein, we investigated whether Cathepsin B is involved in cardiomyocyte apoptosis caused by hyperthermic injury (HI) and heat shock protein (HSP)-70 protects these cells from HI-induced apoptosis mediated by Cathepsin. HI was produced in H9C2 cells by putting them in a circulating 43 °C water bath for 120 min, whereas preinduction of HSP-70 was produced in H9C2 cells by mild heat preconditioning (or putting them in 42 °C water bath for 30 min) 8 h before the start of HI. It was found that HI caused both cardiomyocyte apoptosis and increased Cathepsin B activity in H9C2 cells. E-64-c, in addition to reducing Cathepsin B activity, significantly attenuated HI-induced cardiomyocyte apoptosis (evidenced by increased apoptotic cell numbers, increased tuncated Bid (t-Bid), increased cytochrome C, increased caspase-9/-3, and decreased Bcl-2/Bax) in H9C2 cells. In addition, preinduction of HSP-70 by mild heat preconditioning or inhibition of HSP-70 by Tripolide significantly attenuated or exacerbated respectively both the cardiomyocyte apoptosis and increased Cathepsin B activity in H9C2 cells. Furthermore, the beneficial effects of pre-induction of HSP-70 by mild heat production in reducing both cardiomyocyte apoptosis and increased Cathepsin B activity caused by HI can be significantly reduced by Triptolide preconditioning. These results indicate that Cathepsin B is involved in HI-induced cardiomyocyte apoptosis in H9C2 cells and HSP-70 protects these cells from HI-induced cardiomyocyte apoptosis through Cathepsin B pathways.

原文英語
頁（從 - 到）1571-1580
頁數10
期刊Apoptosis
卷19
發行號11
DOIs
出版狀態已發佈 - 十月 14 2014

指紋

Cathepsin B
HSP70 Heat-Shock Proteins
Cardiac Myocytes
Shock
Hot Temperature
Apoptosis
Wounds and Injuries
Baths
Cathepsins
Cysteine Proteases
Caspase 9
Water
Thermogenesis
Cytochromes
Caspase 3
Cell Count
Cells

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Biochemistry, medical
  • Cancer Research
  • Pharmaceutical Science
  • Pharmacology
  • Medicine(all)

引用此文

Cathepsin B is involved in the heat shock induced cardiomyocytes apoptosis as well as the anti-apoptosis effect of HSP-70. / Hsu, Shu Fen; Hsu, Chuan Chih; Cheng, Bor Chih; Lin, Cheng Hsien.

於: Apoptosis, 卷 19, 編號 11, 14.10.2014, p. 1571-1580.

研究成果: 雜誌貢獻 › 文章

Hsu, SF, Hsu, CC, Cheng, BC & Lin, CH 2014, 'Cathepsin B is involved in the heat shock induced cardiomyocytes apoptosis as well as the anti-apoptosis effect of HSP-70', Apoptosis, 卷 19, 編號 11, 頁 1571-1580. https://doi.org/10.1007/s10495-014-1033-9
Hsu SF, Hsu CC, Cheng BC, Lin CH. Cathepsin B is involved in the heat shock induced cardiomyocytes apoptosis as well as the anti-apoptosis effect of HSP-70. Apoptosis. 2014 10月 14;19(11):1571-1580. https://doi.org/10.1007/s10495-014-1033-9
Hsu, Shu Fen ; Hsu, Chuan Chih ; Cheng, Bor Chih ; Lin, Cheng Hsien. / Cathepsin B is involved in the heat shock induced cardiomyocytes apoptosis as well as the anti-apoptosis effect of HSP-70. 於: Apoptosis. 2014 ; 卷 19, 編號 11. 頁 1571-1580.
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AU - Hsu, Chuan Chih

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AU - Lin, Cheng Hsien

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AB - Cathepsin B is one of the major lysosomal cysteine proteases that plays an important role in apoptosis. Herein, we investigated whether Cathepsin B is involved in cardiomyocyte apoptosis caused by hyperthermic injury (HI) and heat shock protein (HSP)-70 protects these cells from HI-induced apoptosis mediated by Cathepsin. HI was produced in H9C2 cells by putting them in a circulating 43 °C water bath for 120 min, whereas preinduction of HSP-70 was produced in H9C2 cells by mild heat preconditioning (or putting them in 42 °C water bath for 30 min) 8 h before the start of HI. It was found that HI caused both cardiomyocyte apoptosis and increased Cathepsin B activity in H9C2 cells. E-64-c, in addition to reducing Cathepsin B activity, significantly attenuated HI-induced cardiomyocyte apoptosis (evidenced by increased apoptotic cell numbers, increased tuncated Bid (t-Bid), increased cytochrome C, increased caspase-9/-3, and decreased Bcl-2/Bax) in H9C2 cells. In addition, preinduction of HSP-70 by mild heat preconditioning or inhibition of HSP-70 by Tripolide significantly attenuated or exacerbated respectively both the cardiomyocyte apoptosis and increased Cathepsin B activity in H9C2 cells. Furthermore, the beneficial effects of pre-induction of HSP-70 by mild heat production in reducing both cardiomyocyte apoptosis and increased Cathepsin B activity caused by HI can be significantly reduced by Triptolide preconditioning. These results indicate that Cathepsin B is involved in HI-induced cardiomyocyte apoptosis in H9C2 cells and HSP-70 protects these cells from HI-induced cardiomyocyte apoptosis through Cathepsin B pathways.

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KW - Heat shock protein 70

KW - Hyperthermic injury

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