PINCH1 plays an essential role in early murine embryonic development but is dispensable in ventricular cardiomyocytes

被引：81

作者：

Liang, XQ ^{[1
]}

Zhou, Q ^{[1
]}

Li, XD ^{[1
]}

Sun, YF ^{[1
]}

Lu, M ^{[1
]}

Dalton, N ^{[1
]}

Ross, J ^{[1
]}

Chen, J ^{[1
]}

机构：

[1] Univ Calif San Diego, Sch Med, Dept Med, Inst Mol Med, La Jolla, CA 92093 USA

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2005年 / 25卷 / 08期

关键词：

D O I：

10.1128/MCB.25.8.3056-3062.2005

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

PINCH1, an adaptor protein composed of five LIM domains, mediates protein-protein interactions and functions as a component of the integrin-integrin-linked kinase (ILK) complex. The integrin-ILK signaling complex plays a pivotal role in cell motility, proliferation, and survival during embryonic development of many animal species. To elucidate the physiological function of PINCH1 in mouse embryonic development, we have deleted the mouse PINCH1 gene by homologous recombination. Mice heterozygous for PINCH1 are viable and indistinguishable from wild-type littermates. However, no viable homozygous offspring were observed from PINCH1(+/-) intercrosses. Histological analysis of homozygous mutant embryos revealed that they had a disorganized egg cylinder by E5.5, which degenerated by E6.5. Furthermore, E5.5 PINCH1(-/-) embryos exhibited decreased cell proliferation and excessive cell death. We have also generated and analyzed mice in which PINCH1 has been specifically deleted in ventricular cardiomyocytes. These mice exhibit no basal phenotype, with respect to mouse survival, cardiac histology, or cardiac function as measured by echocardiography. Altogether, these data indicate that PINCH1 plays an essential role in early murine embryonic development but is dispensable in ventricular cardiomyocytes.

引用

页码：3056 / 3062

页数：7

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