Human umbilical vein endothelium-derived cells retain potential to differentiate into smooth muscle-like cells

被引:75
作者
Ishisaki, A
Hiyashi, H
Li, AJ
Imamura, T
机构
[1] Natl Inst Adv Ind Sci & Technol, Age Dimens Res Ctr, Tsukuba, Ibaraki 3058566, Japan
[2] Univ Tsukuba, Inst Biol Sci, Tsukuba, Ibaraki 3058572, Japan
关键词
D O I
10.1074/jbc.M207329200
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
Mouse embryonic stem-derived cells were recently shown to differentiate into endothelial and smooth muscle cells. In the present study, we investigated whether human umbilical vein endothelium-derived cells retain the potential to differentiate into smooth muscle cells. Examination of biochemical markers, including basic calponin, SM22alpha, prostaglandin E synthase, von Willebrand factor, and PECAM-1, as well as cell contractility, showed that whereas endothelium-derived cells cultured with fibroblast growth factor can be characterized as endothelial cells, when deprived of fibroblast growth factor, a significant fraction differentiates into smooth muscle-like cells. Reapplication of fibroblast growth factor reversed this differentiation. Activin A was up-regulated in fibroblast growth factor-deprived, endothelium-derived cells; moreover, the inhibitory effects of exogenous follistatin and overexpressed Smad7 on smooth muscle-like differentiation confirmed that the differentiation was driven by activin A signaling. These findings indicate that when deprived of fibroblast growth factor, human umbilical vein endothelium-derived cells are capable of differentiating into smooth muscle-like cells through activin A-induced, Smad-dependent signaling, and that maintenance of the endothelial cell phenotype and differentiation into smooth muscle-like cells are reciprocally controlled by fibroblast growth factor-1 and activin A.
引用
收藏
页码:1303 / 1309
页数:7
相关论文
共 53 条
[1]   APOPTOSIS OF VASCULAR ENDOTHELIAL-CELLS BY FIBROBLAST GROWTH-FACTOR DEPRIVATION [J].
ARAKI, S ;
SHIMADA, Y ;
KAJI, K ;
HAYASHI, H .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 168 (03) :1194-1200
[2]  
ARCINIEGAS E, 1992, J CELL SCI, V103, P521
[3]   Transcription activation of FLRG and follistatin by activin A, through Smad proteins, participates in a negative feedback loop to modulate activin A function [J].
Bartholin, L ;
Maguer-Satta, V ;
Hayette, S ;
Martel, S ;
Badoux, M ;
Corbo, L ;
Magaud, JP ;
Rimokh, R .
ONCOGENE, 2002, 21 (14) :2227-2235
[4]  
Carballada R, 2001, DEVELOPMENT, V128, P35
[5]   Mechanisms of angiogenesis and arteriogenesis [J].
Carmeliet, P .
NATURE MEDICINE, 2000, 6 (04) :389-395
[6]  
Cox CM, 2000, DEV DYNAM, V218, P371, DOI 10.1002/(SICI)1097-0177(200006)218:2<371::AID-DVDY10>3.3.CO
[7]  
2-Q
[8]  
Debiais F, 2001, J CELL BIOCHEM, V81, P68, DOI 10.1002/1097-4644(20010401)81:1<68::AID-JCB1024>3.0.CO
[9]  
2-S
[10]   Embryonic endothelial cells transdifferentiate into mesenchymal cells expressing smooth muscle actins in vivo and in vitro [J].
DeRuiter, MC ;
Poelmann, RE ;
VanMunsteren, JC ;
Mironov, V ;
Markwald, RR ;
GittenbergerdeGroot, AC .
CIRCULATION RESEARCH, 1997, 80 (04) :444-451