The dynamic expression of tenascin-C and tenascin-X during early heart development in the mouse
The dynamic expression of tenascin-C and tenascin-X during early heart development in the mouse
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DOI：
10.1046/j.1432-0436.2003.7104506.x
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发表时间：
2003-06-01
期刊：
影响因子：
2.9
通讯作者：
Yoshida, T
中科院分区：
文献类型：
--
作者：
Imanaka-Yoshida, K;Matsumoto, K;Yoshida, T
腱生蛋白-C（tenascin-C，TNC）是细胞外基质蛋白家族中的一员，在胚胎发育、伤口愈合、癌症侵袭和组织再生期间以与组织重塑相关的时空限制模式表达。另一种形式，腱生蛋白-X（TNX），在大多数组织中发现，但最主要的是在心脏和肌肉中，通常与TNC互补。目前的分析表明，它们的表达在心脏发育早期，使用小鼠线含有lacZ基因靶向TNC位点，通过RT-PCR，免疫组织化学和原位杂交。TNC在心脏发育的重要阶段瞬时表达：（1）E7.5 - 8.5心前中胚层细胞分化为心肌细胞和内皮细胞，（2）E8.5 - 12流出道心肌细胞，（3）E9.5 - 13内皮细胞形成垫状组织，（4）E9.5 - 13心肌细胞形成垫状组织，（5）E9.5 - 13心肌细胞形成垫状组织，（6）E9.5 - 13心肌细胞形成垫状组织。（4）E9.5时，心前外膜器官（PEO）中的间充质细胞，它们是冠状血管的前体。当PEO细胞转移到心脏表面时，TNC的表达下调，而TNX在E11时上调。最初，房室沟和心房周围的心外膜细胞开始表达TNX。TNX阳性细胞随后逐渐遍布心脏的整个表面，并侵入心肌中并形成原始血管通道。尽管在心脏发生过程中的重要部位和步骤的表达受到限制，但TNC缺陷小鼠的心脏发育正常。TNC基因敲除小鼠和野生型小鼠的TNX表达模式无差异。这些结果表明;（1）TNC在心肌细胞分化和心脏早期形态发生中起重要作用;（2）TNX参与冠状动脉血管生成;（3）TNX不能代偿TNC的丢失。
One of a family of extracellular matrix proteins, tenascin-C (TNC) is expressed in a spatiotemporally restricted pattern associated with tissue remodeling during embryonic development, wound healing, cancer invasion and tissue regeneration. Another form, tenascin-X (TNX), is found in most tissues but most predominantly in heart and muscle, often complementarily to TNC. The present analysis demonstrated their expression during early heart development, using mouse lines containing the lacZ gene targeted to the TNC locus, by RT-PCR, immunohistochemistry, and in situ hybridization. TNC was transiently expressed at important steps during heart development: (1) precardiac mesodermal cells differentiating to cardiomyocytes and endocardial cells at E 7.5 - 8.5; (2) cardiomyocytes in the outflow tract at E 8.5 - 12; (3) endocardial cells forming cushion tissue at E 9.5 - 13; and (4) mesenchymal cells in the proepicardial organ (PEO), the precursors of coronary vessels, at E 9.5. When PEO cells were transferred onto the heart surface, the expression of TNC was downregulated, while TNX was upregulated at E 11. Initially, epicardial cells around the AV groove and atrium started to express TNX. TNX-positive cells then gradually spread all over the entire surface of the heart and invaded and formed primitive vascular channels in the myocardium. Despite restricted expression at important sites and steps during cardiogenesis, the hearts of TNC deficient mice developed normally. No difference in the expression pattern of TNX were observed in TNC knockout and wild mice. These results suggest; (1) TNC could play important roles in the differentiation of cardiomyocytes and the early morphogenesis of the heart; (2) TNX could be involved in coronary vasculogenesis; (3) TNX does not compensate for the loss of TNC.