p53基因导致心肌细胞凋亡及其机制探讨

Wild type p53 gene transference induces apoptosis in cultured rabbit cardiomyocytes

目的 探讨野生型p5 3基因与心肌细胞凋亡的关系及其可能的发生机制。方法 把野生型p5 3基因重组腺病毒转入体外培养的心肌细胞中 ,采用流式细胞计数仪 (FCM) ,透射电镜等实验方法检测细胞凋亡并分析其作用机制。结果 重组腺病毒能有效地将p5 3基因转入心肌细胞中 ;转入的p5 3基因可以导致心肌细胞体积变小、胞浆浓缩、核固缩、染色质边集 ,引起细胞G1期阻滞。结论 野生型p5 3基因可以导致心肌细胞凋亡 ,并能影响细胞周期。以上结果为进一步研究心肌疾病的发病机制及其治疗提供了重要的实验依据。

Objective To study the relation between wild type p53 gene and apoptosis of cardiomyocytes in rabbits and possible mechanism.Methods We transfered wild type p53 gene mediated by recombinant adenovirus vector into cardiomyocytes. Apoptosis was verified by electron microscopy and flow-type cell counter. Results p53 gene could be quickly and effectively transfered into the cardiomyocytes by recombinant adenovirus, transfered p53 gene let to plasmatic concentration,nuclear contraction and G 1 arrest.Conclusion p53 gene could cause apoptosis of the cells and affect myltiplication cycle. This study provided important reliance for gene therapy of myocardiac diseases.