Overexpression of CyclinA2 ameliorates hypoxia-impaired proliferation of cardiomyocytes.

摘要: Hypoxia is a primary mediator for cell survival, and has been reported to inhibit cardiomyocyte proliferation in fetal neonatal hearts. CyclinA2 key regulator of proliferation. Whether affects hypoxic conditions remains unexamined. This study was designed investigate the roles expression on hypoxia-impaired Cardiomyocytes were isolated from rats randomly separated into six groups: Control, hypoxia, enhanced green fluorescent protein (EGFP)-Adv, EGFP-Ccna2, EGFP-Adv + hypoxia EGFP-Ccna2 hypoxia. The cells control group cultured general incubator; placed chamber 12 h; groups separately transfected with EGFP-adenovirus capsids or cDNA 18 h, then incubator an additional h. measured using immunochemical staining western blot analysis, counting kit 8. GFP fluorescence indicated high transfection efficiency (>80%), showed that mainly distributed nucleus. downregulated following exposure Cardiomyocyte also significantly decreased However, compared group, markedly increased group. Furthermore, These findings indicate upregulation improves conditions.