Loss of HB-EGF in smooth muscle or endothelial cell lineages causes heart malformation

被引：17

作者：

Nanba, Daisuke

Kinugasa, Yumi

Morimoto, Chie

Koizumi, Michiko

Yamamura, Hisako

Takahashi, Katsuhito

Takakura, Nobuyuki

Mekada, Eisuke

Hashimoto, Koji

Higashiyama, Shigeki ^{[1
]}

机构：

[1] Ehime Univ, Grad Sch Med, Dept Biochem & Mol Genet, Toon, Ehime 7910295, Japan

[2] Ehime Univ, Grad Sch Med, Dept Dermatol, Toon, Ehime 7910295, Japan

[3] Osaka Med Ctr Canc & Cardiovasc Dis, Dept Med, Osaka 5378511, Japan

[4] Osaka Univ, Res Inst Microbial Dis, Dept Signal Transduct, Osaka 5650871, Japan

[5] Osaka Univ, Res Inst Microbial Dis, Dept Cell Biol, Osaka 5650871, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 350卷 / 02期

关键词：

cardiac hypertrophy; conditional knockout; HB-EGF; heart valves; heart failure;

D O I：

10.1016/j.bbrc.2006.09.060

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：

Epidermal growth factor (EGF) and ErbB family molecules play a role in heart development and function. To investigate the role of EGF family member, heparin-binding EGF-like growth factor (HB-EGF) in heart development, smooth muscle and endothelial cell lineage-specific HB-EGF knockout mice were generated using the Cre/loxP system in combination with the SM22 alpha or TIE2 promoter. HBEGF knockout mice displayed enlarged heart valves, and over half of these mice died during the first postnatal week, while survivors showed cardiac hypertrophy. These results suggest that expression of HB-EGF in smooth muscle and/or endothelial cell lineages is essential for proper heart development and function in mice. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：315 / 321

页数：7

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