Mab21l2 is essential for embryonic heart and liver development.
Mab21l2 is essential for embryonic heart and liver development.
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MAB21L2对于胚胎心脏和肝脏发育至关重要。
DOI：
10.1371/journal.pone.0032991
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Takahashi N
中科院分区：
文献类型：
--
作者：
Saito Y;Kojima T;Takahashi N
在小鼠胚胎发育过程中，心脏和肝脏的正确形成尤其重要，对胚胎的存活至关重要。在这项研究中，我们发现Mab21l2在小梁和致密心肌中表达，Mab21l2的缺失导致小梁心肌减少，致密心肌变薄。Mab21l2缺陷的胚胎心脏降低了调控细胞增殖和心肌细胞凋亡的基因的表达。这些结果表明，Mab21l2通过调节这些基因的表达而在心脏发育过程中发挥作用。Mab21l2在横隔间充质(STM)也有表达。心外膜前体细胞定位于心前膜的前表面，心外膜细胞迁移到心脏表面形成心外膜，在心脏发育过程中起重要作用。STM的其余部分对于肝母细胞的生长和生存是必不可少的，肝母细胞是肝细胞和胆管细胞的双潜能前体细胞。Mab21l2基因缺陷胚胎的心前膜细胞存在细胞增殖缺陷，导致心包膜小，心外膜细胞迁移所必需的α-4整合素表达下调，提示心外膜细胞迁移过程中存在缺陷。在Mab21l2缺陷的胚胎中，心外膜形成有缺陷，提示Mab21l2通过调节心外膜细胞的增殖和迁移过程在心外膜形成过程中发挥重要作用。Mab21l2基因缺陷的胚胎还显示肝母细胞周围的STM发育不良，肝母细胞增殖减少，导致肝脏形态发生缺陷的丧失。这些发现表明，Mab21l2通过STM的形成在心脏和肝脏的发育中起着至关重要的作用。
During mouse embryogenesis, proper formation of the heart and liver is especially important and is crucial for embryonic viability. In this study, we showed that Mab21l2 was expressed in the trabecular and compact myocardium, and that deletion of Mab21l2 resulted in a reduction of the trabecular myocardium and thinning of the compact myocardium. Mab21l2-deficient embryonic hearts had decreased expression of genes that regulate cell proliferation and apoptosis of cardiomyocytes. These results show that Mab21l2 functions during heart development by regulating the expression of such genes. Mab21l2 was also expressed in the septum transversum mesenchyme (STM). Epicardial progenitor cells are localized to the anterior surface of the STM (proepicardium), and proepicardial cells migrate onto the surface of the heart and form the epicardium, which plays an important role in heart development. The rest of the STM is essential for the growth and survival of hepatoblasts, which are bipotential progenitors for hepatocytes and cholangiocytes. Proepicardial cells in Mab21l2-deficient embryos had defects in cell proliferation, which led to a small proepicardium, in which α4 integrin expression, which is essential for the migration of proepicardial cells, was down-regulated, suggesting that defects occurred in its migration. In Mab21l2-deficient embryos, epicardial formation was defective, suggesting that Mab21l2 plays important roles in epicardial formation through the regulation of the cell proliferation of proepicardial cells and the migratory process of proepicardial cells. Mab21l2-deficient embryos also exhibited hypoplasia of the STM surrounding hepatoblasts and decreased hepatoblast proliferation with a resultant loss of defective morphogenesis of the liver. These findings demonstrate that Mab21l2 plays a crucial role in both heart and liver development through STM formation.
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