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目的探讨磷酸化ERK和p38MAPK信号通路在小儿血管瘤增生、消退中的作用。方法应用免疫组化SP法检测47例血管瘤(增殖期26例、消退期21例)组织中磷酸化ERK和p38MAPK的表达情况。结果磷酸化ERK阳性定位于细胞核,其在增殖期和消退期的阳性细胞指数分别为(67.71±12.68)%和(21.54±6.85)%;磷酸化p38MAPK阳性定位于细胞核,其在增殖期和消退期的阳性细胞指数分别为(83.78±5.25)%和(57.79±7.63)%;增生期磷酸化ERK与p38MAPK阳性表达呈正相关,而消退期呈负相关。结论磷酸化ERK和p38MAPK参与血管瘤的增生、消退过程;ERK通路可介导内皮细胞的增生和存活,而p38MAPK可能主要在消退期传递内、外源性凋亡信号,诱导内皮细胞凋亡。
Objective To investigate the role of phosphorylated ERK and p38 MAPK signaling in the proliferation and regression of pediatric hemangiomas. Methods The expressions of phosphorylated ERK and p38 MAPK in 47 hemangiomas (26 proliferative and 21 regression) were detected by immunohistochemical SP method. Results Phosphorylated ERK was localized in the nucleus and its positive cell index was (67.71 ± 12.68)% and (21.54 ± 6.85)%, respectively. The phosphorylated p38 MAPK was localized in the nucleus and proliferated and dissipated (83.78 ± 5.25)% and (57.79 ± 7.63)%, respectively. The positive expression of phosphorylated ERK and p38MAPK in proliferative phase was positively correlated with that in extinction phase. Conclusions Phosphorylation of ERK and p38MAPK are involved in the proliferation and regression of hemangiomas. The ERK pathway may mediate the proliferation and survival of endothelial cells. However, p38MAPK may transmit endogenous and extrinsic apoptotic signals and induce the apoptosis of endothelial cells mainly during extinction.