Generation of Smad7(-Cre) recombinase mice: A useful tool for the study of epithelial-mesenchymal transformation within the embryonic heart.
Generation of Smad7(-Cre) recombinase mice: A useful tool for the study of epithelial-mesenchymal transformation within the embryonic heart.
复制标题
Smad7(-Cre) 重组酶小鼠的产生：研究胚胎心脏内上皮间质转化的有用工具。
DOI：
10.1002/dvg.20524
复制
发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Conway,SimonJ
中科院分区：
文献类型：
--
作者：
Snider,Paige;Tang,Sunyong;Lin,Goldie;Wang,Jian;Conway,SimonJ
Smad7可以被各种转化生长因子- β超家族配体诱导并负向调节其信号传导，从而以负的自分泌反馈方式起作用。先前的分析表明，尽管Smad7广泛表达，但它主要存在于血管内皮中。由于在覆盖心脏房室（AV）缓冲层的心内膜细胞中，由一个新的4.3 kb Smad7启动子驱动的限制性时空报告基因表达；我们假设转基因creline将被证明对心内膜缓冲和瓣膜形成的分析有用。在这里，我们描述了一个小鼠系Smad7Cre，其中Cre在心流出液和房室心内膜垫中都有强烈表达。此外，由于心内膜细胞被认为至少在一定程度上有助于心内膜缓冲间质的形成，我们将smad7cremice与表达osa26egfp -白喉毒素A -的小鼠杂交，以从基因上清除表达esmad7cremice的细胞。消融smad7creccells导致E11.5和大部分无细胞心内膜缓冲的胚胎死亡。创世纪47:46 - 475,2009。©2009 Wiley‐Liss, Inc。
Smad7 can be induced by various transforming growth factor‐β superfamily ligands and negatively modulates their signaling, thus acting in a negative, autocrine feedback manner. Previous analyses have demonstrated that although Smad7 is widely expressed, it is predominantly found in the vascular endothelium. Because of the restricted spatiotemporal reporter expression driven via a novel 4.3 kb Smad7 promoter in endocardial cells overlying the hearts atrioventricular (AV) cushions; we hypothesized that a transgenicCreline would prove useful for the analysis of endocardial cushion and valve formation. Here we describe a mouse line,Smad7Cre, where Cre is robustly expressed within both cardiac outflow and AV endocardial cushions. Additionally, as endocardial cells are thought to contribute at least in part to the formation of the endocardial cushion mesenchyme, we crossed theSmad7Cremice to theROSA26eGFP‐DTAdiphtheria toxin A‐expressing mice in order to genetically ablateSmad7Creexpressing cells. Ablation ofSmad7Crecells resulted in embryonic lethality by E11.5 and largely acellular endocardial cushions. genesis 47:469–475, 2009. © 2009 Wiley‐Liss, Inc.