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小鼠胶原蛋白I基因的胚胎致死性突变导致血管破裂,并与红细胞生成和间充质细胞死亡有关。

Embryonic lethal mutation in mouse collagen I gene causes rupture of blood vessels and is associated with erythropoietic and mesenchymal cell death.

作者信息

Löhler J, Timpl R, Jaenisch R

出版信息

Cell. 1984 Sep;38(2):597-607. doi: 10.1016/0092-8674(84)90514-2.

DOI:10.1016/0092-8674(84)90514-2
PMID:6467375
Abstract

The role of collagen I for midgestation development was studied in homozygous Mov 13 embryos, which cannot synthesize alpha 1(1) mRNA as a result of insertional mutagenesis and most of which die between day 12 and 14 of gestation. No type I collagen was detected in mutant embryos, while the distribution of other collagens, laminin, and fibronectin was not affected. Mutant embryos develop normally up to day 12 of gestation, suggesting that collagen I has no essential role in the early phase of morphogenesis. The first pathological events were detected in hemopoietic cells of the liver, followed by necroses of mesenchymal cells in other parts of the embryo. The sudden death is caused by the rupture of a major blood vessel, indicating an important role for collagen I in establishing the mechanical stability of the circulatory system. Our results furthermore suggest that complex cell interactions in embryonic development such as those in early hemopoiesis may depend on the presence of collagen type I.

摘要

在纯合Mov 13胚胎中研究了I型胶原蛋白在妊娠中期发育中的作用,这些胚胎由于插入诱变而无法合成α1(1) mRNA,并且大多数在妊娠第12天至14天之间死亡。在突变胚胎中未检测到I型胶原蛋白,而其他胶原蛋白、层粘连蛋白和纤连蛋白的分布未受影响。突变胚胎在妊娠第12天之前发育正常,这表明I型胶原蛋白在形态发生的早期阶段没有重要作用。首先在肝脏的造血细胞中检测到病理事件,随后胚胎其他部位的间充质细胞发生坏死。猝死是由一条主要血管破裂引起的,这表明I型胶原蛋白在建立循环系统的机械稳定性方面具有重要作用。我们的结果还表明,胚胎发育中的复杂细胞相互作用,如早期造血过程中的相互作用,可能依赖于I型胶原蛋白的存在。

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