Snrk-1 is involved in multiple steps of angioblast development and acts via notch signaling pathway in artery-vein specification in vertebrates

被引：27

作者：

Chun, Chang Z. ^{[1
]}

Kaur, Sukhbir ^{[2
]}

Samant, Ganesh V. ^{[1
]}

Wang, Ling ^{[3
]}

Pramanik, Kallal ^{[1
]}

Garnaas, Maija K. ^{[1
]}

Li, Keguo ^{[1
]}

Field, Lyndsay ^{[4
]}

Mukhopadhyay, Debabrata ^{[3
]}

Ramchandran, Ramani ^{[1
]}

机构：

[1] Med Coll Wisconsin, Dept Pediat, Translat & Biomed Res Ctr, CRI Dev Vasc Biol Program, Milwaukee, WI 53226 USA

[2] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA

[3] Mayo Clin, Coll Med, Dept Biochem & Mol Biol, Rochester, MN USA

[4] Univ Massachusetts Dartmouth, N Dartmouth, MA USA

来源：

BLOOD | 2009年 / 113卷 / 05期

基金：

美国国家卫生研究院;

关键词：

VASCULAR MALFORMATIONS; ENDOTHELIAL-CELLS; OVEREXPRESSION; VASCULOGENESIS; ANGIOGENESIS; EXPRESSION; GRIDLOCK; PROTEIN; GENES;

D O I：

10.1182/blood-2008-06-162156

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

In vertebrates, molecular mechanisms dictate angioblasts' migration and subsequent differentiation into arteries and veins. In this study, we used a microarray screen to identify a novel member of the sucrose nonfermenting related kinase (snrk-1) family of serine/threonine kinases expressed specifically in the embryonic zebrafish vasculature and investigated its function in vivo. Using gain- and loss-of-function studies in vivo, we show that Snrk-1 plays an essential role in the migration, maintenance, and differentiation of angioblasts. The kinase function of Snrk-1 is critical for migration and maintenance, but not for the differentiation of angioblasts. In vitro, snrk-1 knockdown endothelial cells show only defects in migration. The snrk-1 gene acts down-stream or parallel to notch and upstream of gridlock during artery-vein specification, and the human gene compensates for zebrafish snrk-1 knockdown, suggesting evolutionary conservation of function. (Blood. 2009; 113: 1192-1199)

引用

页码：1192 / 1199

页数：8

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