Attenuating heat-induced cellular autophagy, apoptosis and damage in H9c2 cardiomyocytes by pre-inducing HSP70 with heat shock preconditioning

doi:10.3109/02656736.2013.777853

CNU IR > College of Sustainable Environment and Recreation > Dept. of Recreation and Health-Care Management > Periodical Articles > Item 310902800/27782

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/27782

Title:	Attenuating heat-induced cellular autophagy, apoptosis and damage in H9c2 cardiomyocytes by pre-inducing HSP70 with heat shock preconditioning
Authors:	Hsu, Shu-Fen Chao, Chien-Ming Huang, Wu-Tein Lin, Mao-Tsun Cheng, Bor-Chih
Contributors:	休閒保健管理系
Keywords:	Apoptosis Autophagy Cardiac Myocytes Heat Shock Preconditioning Heat Shock Protein 70
Date:	2013-07
Issue Date:	2014-05-26 10:43:27 (UTC+8)
Publisher:	Informa Healthcare
Abstract:	Purpose: We sought to assess whether heat-induced autophagy, apoptosis and cell damage in H9c2 cells can be affected by pre-inducing HSP70 (heat shock protein 70).Materials and methods: Cell viability was determined using 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl tetrazolium bromide staining and a lactate dehydrogenase assay. Apoptosis was evidenced using both flow cytometry and counting caspase-3 positive cells, whereas autophagy was evidenced by the increased LC3-II expression and lysosomal activity.Results: The viability of H9c2 cells was temperature-dependently (40-44 degrees C) and time-dependently (90-180 min) significantly (p<0.05) reduced by severe heat, which caused cell damage, apoptosis and autophagy. Heat-induced cell injury could be attenuated by pretreatment with 3-methylademine (an autophagy inhibitor) or Z-DEVD-FMK (a caspase-3 inhibitor). Neither apoptosis nor autophagy over the levels found in normothermic controls was induced in heat-shock preconditioned controls (no subsequent heat injury). The beneficial effects of mild heat preconditioning (preventing heat-induced cell damage, apoptosis and autophagy) were significantly attenuated by inhibiting HSP70 overexpression with triptolide (Tripterygium wilfordii) pretreatment.Conclusion: We conclude that pre-inducing HSP70 attenuates heat-stimulated cell autophagy, apoptosis and damage in the heart. However, this requires in vivo confirmation.
Relation:	International Journal of Hyperthermia, v.29 n.3 pp.239-247
Appears in Collections:	[Dept. of Recreation and Health-Care Management] Periodical Articles

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