Kinetic expression of platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) during embryonic stem cell differentiation

被引：40

作者：

Li, ZJ

Wang, ZZ

Zheng, YZ

Xu, B

Yang, RC

Scadden, DT

Han, ZC

机构：

[1] Chinese Acad Med Sci, Inst Hematol, State Key Lab Expt Hematol, Natl Res Ctr Stem Cell Engn & Technol, Tianjin 300020, Peoples R China

[2] Blood Dis Hosp, Chinese Acad Med Sci, Tianjin 300020, Peoples R China

[3] Peking Union Med Coll, Tianjin 300020, Peoples R China

[4] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02115 USA

来源：

JOURNAL OF CELLULAR BIOCHEMISTRY | 2005年 / 95卷 / 03期

关键词：

PECAM-1/CD31; embryonic stem cells; alternative splicing; vasculogenesis; angiogenesis; endothelial differentiation;

D O I：

10.1002/jcb.20436

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：

Platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) is widely used as a marker during vasculogenesis and angiogenesis from embryonic stem (ES) cells. However, the expression of PECAM-1 isoforms in ES cells has not been determined. The present study was designed to determine the role of PECAM-1 isoforms during in vitro enclothelial differentiation of ES cells. It was found that undifferentiated ES cells expressed high level of PECAM-1, which primarily located at cell-cell junction, but the expression of PECAM-1 was sharply down-regulated during early ES cell differentiation. In addition, undifferentiated ES cells were found the expressed all eight known alternatively spliced PECAM-1 isoforms, among them the expression of PECAM-1 isoforms lacking exon 15 or 14&15 was predominant. Quantitative analysis revealed a significant increase in the expression of PECAM-1 isoform lacking exon 12&14&15 as vascular development of ES cells. These results indicate a constitutive expression of PECAM-1 in undifferentiated murine ES cells and suggest a developmental role of PECAM-1 isoform changes during vasculogenesis and angiogenesis.J. Cell. Biochem. (c) 2005 Wiley-Liss, Inc.

引用

页码：559 / 570

页数：12

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