The orphan nuclear receptor COUP-TFII is required for angiogenesis and heart development

被引：418

作者：

Pereira, FA ^{[1
]}

Qiu, YH ^{[1
]}

Zhou, G ^{[1
]}

Tsai, MJ ^{[1
]}

Tsai, SY ^{[1
]}

机构：

[1] Baylor Coll Med, Dept Cell Biol, Houston, TX 77030 USA

来源：

GENES & DEVELOPMENT | 1999年 / 13卷 / 08期

关键词：

angiogenesis; heart defects; COUP-TFII; nuclear receptors;

D O I：

10.1101/gad.13.8.1037

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The embryonic expression of COUP-TFII, an orphan nuclear receptor, suggests that it may participate in mesenchymal-epithelial interactions required for organogenesis. Targeted deletion of the COUP-TFII gene results in embryonic lethality with defects in angiogenesis and heart development. COUP-TFII mutants are defective in remodeling the primitive capillary plexus into large and small microcapillaries. In the COUP-TFII mutant heart, the atria and sinus venosus fail to develop past the primitive tube stage. Reciprocal interactions between the endothelium and the mesenchyme in the vascular system and heart are essential for normal development of these systems. In fact, the expression of Angiopoietin-1, a proangiogenic soluble factor thought to mediate the mesenchymal-endothelial interactions during heart development and vascular remodeling, is down-regulated in COUP-TFII mutants. This down-regulation suggests that COUP-TFII may be required for bidirectional signaling between the endothelial and mesenchymal compartments essential for proper angiogenesis and heart development.

引用

页码：1037 / 1049

页数：13

共 49 条

[1]

BALDWIN HS, 1994, DEVELOPMENT, V120, P2539

[2]

Chen JN, 1996, DEVELOPMENT, V123, P293

[3] Isolation of Angiopoietin-1, a ligand for the TIE2 receptor, by secretion-trap expression cloning [J].

Davis, S ;

Aldrich, TH ;

Jones, PF ;

Acheson, A ;

Compton, DL ;

Jain, V ;

Ryan, TE ;

Bruno, J ;

Radziejewski, C ;

Maisonpierre, PC ;

Yancopoulos, GD .

CELL, 1996, 87 (07) :1161-1169

[4] Increased microvascular density and enhanced leukocyte rolling and adhesion in the skin of VEGF transgenic mice [J].

Detmar, M ;

Brown, LF ;

Schön, MP ;

Elicker, BM ;

Velasco, P ;

Richard, L ;

Fukumura, D ;

Monsky, W ;

Claffey, KP ;

Jain, RK .

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1998, 111 (01) :1-6

[5] EXOGENOUS VASCULAR ENDOTHELIAL GROWTH-FACTOR INDUCES MALFORMED AND HYPERFUSED VESSELS DURING EMBRYONIC NEOVASCULARIZATION [J].

DRAKE, CJ ;

LITTLE, CD .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (17) :7657-7661

[6] DOMINANT-NEGATIVE AND TARGETED NULL MUTATIONS IN THE ENDOTHELIAL RECEPTOR TYROSINE KINASE, TEK, REVEAL A CRITICAL ROLE IN VASCULOGENESIS OF THE EMBRYO [J].

DUMONT, DJ ;

GRADWOHL, G ;

FONG, GH ;

PURI, MC ;

GERTSENSTEIN, M ;

AUERBACH, A ;

BREITMAN, ML .

GENES & DEVELOPMENT, 1994, 8 (16) :1897-1909

[7]

FENG JQ, 1995, J BIOL CHEM, V270, P28364, DOI 10.1074/jbc.270.47.28364

[8] Parsing the heart: Genetic modules for organ assembly [J].

Fishman, MC ;

Olson, EN .

CELL, 1997, 91 (02) :153-156

[9]

Fishman MC, 1997, DEVELOPMENT, V124, P2099

[10] A NOVEL VERTEBRATE SVP-RELATED NUCLEAR RECEPTOR IS EXPRESSED AS A STEP GRADIENT IN DEVELOPING RHOMBOMERES AND IS AFFECTED BY RETINOIC ACID [J].

FJOSE, A ;

WEBER, U ;

MLODZIK, M .

MECHANISMS OF DEVELOPMENT, 1995, 52 (2-3) :233-246

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