期刊
INTERNATIONAL JOURNAL OF HYPERTHERMIA
卷 29, 期 3, 页码 239-247出版社
INFORMA HEALTHCARE
DOI: 10.3109/02656736.2013.777853
关键词
Apoptosis; autophagy; cardiac myocytes; heat shock preconditioning; heat shock protein 70
资金
- Taiwan National Science Council [NSC100-2314-B-218-001, NSC99-2314-B-38, 4-004-MY3, NSC99-2314-B-218-006-MY2]
- Taiwan Department of Health [DOH99-TD-B-111-003]
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.
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