Adams R H, Porras A, Alonso G, Jones M, Vintersten K, Panelli S, Valladares A, Perez L, Klein R, Nebreda A R
European Molecular Biology Laboratory, Heidelberg, Germany.
Mol Cell. 2000 Jul;6(1):109-16.
p38alpha MAP kinase is activated in response to many cellular stresses and also regulates the differentiation and/or survival of various cell types in vitro, including skeletal muscle cells and cardiomyocytes. Here we show that targeted inactivation of the mouse p38alpha gene results in embryonic lethality at midgestation correlating with a massive reduction of the myocardium and malformation of blood vessels in the head region. However, this defect appears to be secondary to insufficient oxygen and nutrient transfer across the placenta. When the placental defect was rescued, p38alpha(-/-) embryos developed to term and were normal in appearance. Our results indicate that p38alpha is required for placental organogenesis but is not essential for other aspects of mammalian embryonic development.
p38α丝裂原活化蛋白激酶（MAP激酶）在响应多种细胞应激时被激活，并且在体外还调节包括骨骼肌细胞和心肌细胞在内的各种细胞类型的分化和/或存活。在此我们表明，小鼠p38α基因的靶向失活导致妊娠中期胚胎致死，这与心肌的大量减少以及头部区域血管的畸形有关。然而，这种缺陷似乎继发于跨胎盘的氧气和营养物质转运不足。当胎盘缺陷得到挽救时，p38α基因敲除（p38α-/-）胚胎发育至足月且外观正常。我们的结果表明，p38α是胎盘器官发生所必需的，但对于哺乳动物胚胎发育的其他方面并非必不可少。
