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[慢性阻塞性肺疾病中的细胞凋亡与增殖活性及相关机制]

[Apoptosis versus proliferation activities and relative mechanism in chronic obstructive pulmonary disease].

作者信息

Tao Q, Zhang Z, Xu Y

机构信息

Respiratory Disease Research Laboratory, Tongji Hospital, Tongji Medical University, Wuhan.

出版信息

Zhonghua Yi Xue Za Zhi. 1998 Aug;78(8):574-7.

Abstract

OBJECTIVE

To study the roles of apoptosis and proliferation and relative genes expression in chronic obstructive pulmonary disease (COPD) and pulmonary hypertension.

METHODS

Immunohistochemical technique was used for the detection of cell proliferation and expression of relative genes. In situ end labeling technique was used for the detection of nucleosomal DNA fragmentation of apoptotic cells, and Northern blot for the detection of expression of c-myc, bcl-2 and p53 genes in the lungs with COPD.

RESULTS

Both proliferative cells and apoptotic cells were found in the lungs with COPD or without COPD. In lung tissue with COPD. The proliferation index was increased significantly, whereas the apoptosis index was decreased significantly. Compared with controls, the ratio of proliferation to apoptosis in lungs with COPD was increased by 4 folds, and the expression of c-myc or bcl-2 mRNA was significantly increased by 2.5-3 folds in lungs tissue with COPD. The expression of c-myc and bcl-2 protein was also increased significantly in lungs with COPD, the two antigen were predominantly localized in small pulmonary vessels. The expression of p53 mRNA was significantly decreased by 3 folds in lung tissue with COPD.

CONCLUSION

The abnormality of apoptosis versus proliferation activities induced by c-myc, bcl-2 and p53 genes may contribute to pulmonary vascular structural remodeling in COPD.

摘要

目的

研究细胞凋亡、增殖及相关基因表达在慢性阻塞性肺疾病(COPD)及肺动脉高压中的作用。

方法

采用免疫组织化学技术检测细胞增殖及相关基因表达。采用原位末端标记技术检测凋亡细胞核小体DNA片段化,采用Northern印迹法检测COPD患者肺组织中c-myc、bcl-2和p53基因的表达。

结果

在有或无COPD的肺组织中均发现增殖细胞和凋亡细胞。在COPD肺组织中,增殖指数显著升高,而凋亡指数显著降低。与对照组相比,COPD肺组织中增殖与凋亡的比例增加了4倍,COPD肺组织中c-myc或bcl-2 mRNA的表达显著增加了2.5至3倍。COPD肺组织中c-myc和bcl-2蛋白的表达也显著增加,这两种抗原主要定位于肺小血管。COPD肺组织中p53 mRNA的表达显著降低了3倍。

结论

c-myc、bcl-2和p53基因诱导的凋亡与增殖活性异常可能导致COPD患者肺血管结构重塑。

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