CRYAB protects cardiomyocytes against heat stress by preventing caspase-mediated apoptosis and reducing F-actin aggregation

• DOI: 10.1007/s12192-018-0941-y
• Publication Date: 2018-09-24T01:55:23Z
• Authors: Bin Yin; Shu Tang; Jiao Xu; Jiarui Sun; Xiaohui Zhang; Yubao Li; Endong Bao
• Keywords: Recombination, Genetic; 0301 basic medicine; Transcription, Genetic; Cell Cycle; Apoptosis; Crystallins; Actins; Cell Line; Rats; Protein Aggregates; 03 medical and health sciences; Cytoprotection; Caspases; Animals; Myocytes, Cardiac; Microtubule-Associated Proteins; Heat-Shock Response

CRYAB is a small heat shock protein (sHSP) that has previously been shown to protect the heart against various cellular stresses; however, its precise function in myocardial cell injury caused by stress remains unclear. This study aimed investigate molecular mechanism which protects cardiomyocytes stress. We constructed two H9C2 lines stably express differing degrees: CRYAB-5 and CRYAB-7. Both CRYAB-7 showed significantly reduced granular degeneration vacuolar following compared control cells. In addition, overexpression cells relieved cycle proportion at G0/G1 phase These protective effects were associated with level of expression. Our immunofluorescence analysis could translocate from cytoplasm nucleus under conditions, but co-localized F-actin (which accumulates conditions). Indeed, aggregation Furthermore, overexpressing apoptosis induced stress, likely reducing expression cleaved-caspase 3. Collectively, our results show increases resistance cardiomyocytes, (thus stabilizing cytoskeleton), regulating cycle, preventing caspase-mediated apoptosis.