低氧对培养的肺血管周细胞凋亡的影响

为了研究低氧是否影响肺血管周细胞凋亡并参与腺泡内无肌肺动脉的构型重建， 用ＴＵＮＥＬ法和免疫组化方法， 观察低氧（Ｈ） 组和低氧肺动脉内皮细胞条件培养液（ＨＥＣＣＭ） 组对肺血管周细胞凋亡发生率及抑凋亡基因ｂｃｌ２ 蛋白表达的影响。结果表明：Ｈ组和ＨＥＣＣＭ 组的凋亡指数明显较对照组减小。Ｈ 组和ＨＥＣＣＭ 组ｂｃｌ２ 蛋白的表达量分别是ＮＥＣＣＭ 组的１１７ 倍、１１３ 倍， 是Ｎ组的１３３ 倍、１２７ 倍。提示低氧诱导的抑凋亡基因ｂｃｌ２ 的过度表达， 对周细胞凋亡发生的抑制作用和低氧促进的周细胞增生过程可能都参与无肌肺动脉的构型重建， 与肺动脉高压的形成有关。

THE INFLUENCE OF HYPOXIA ON THE APOPTOSIS OF CULTURED PERICYTES OF PULMONARY VESSEL

In order to study whether hypoxia could influence apoptosis of pulmonary vessel pericytes and take part in structural remodeling of non muscular pulmonary arterioles, the TUNEL(TdT mediated dUTP nick end labeling) technique and immunohistochemical staining were used to observe the effect of hypoxia directly or mediated by pulmonary endothelial cells conditioned medium (group H or group HECCM) on the apoptosis occurrence and bcl 2 protein expression in cultured pericytes. The results showed that apoptosis indexes of pericytes in group H and group HECCM were markedly reduced than the control group. The bcl 2 protein expressive level in group H and group HECCM was 1 17 fold,1 13 fold in comparison with group NECCM, 1 33 fold,1 27 fold in comparison with group N respectively. The results suggested that hypoxia could induce overexpression of bcl 2 gene which suppressed the occurence of pericyte apoptosis and the proliferation of pericytes might take part in the process of vascular remodeling and development of pulmonary hypertension.