Expression of endoglin in human mesangial cells: modulation of extracellular matrix synthesis

被引：67
作者：
Diez-Marques, L
Ortega-Velazquez, R
Langa, C
Rodriguez-Barbero, A
Lopez-Novoa, JM
Lamas, S
Bernabeu, C
机构：
[1] CSIC, Ctr Invest Biol, E-28006 Madrid, Spain
[2] Univ Alcala de Henares, Fac Med, Dept Physiol, Madrid, Spain
[3] Univ Salamanca, Inst Reina Sofia Invest Nefrol, Dept Fisiol & Farmacol, E-37008 Salamanca, Spain
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2002年 / 1587卷 / 01期
关键词：
endoglin; transforming growth factor-beta; renal fibrosis; extracellular matrix; glomerulosclerosis; collagen;
D O I：
10.1016/S0925-4439(02)00051-0
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：
Transforming growth factor-beta (TGF-beta) has been identified as a key mediator of glomerulosclerosis in kidney diseases. Endoglin is a component of the TGF-beta receptor system that is upregulated during glomerulosclerosis, suggesting it role during progression of renal diseases characterized by extracellular matrix (ECM) synthesis and accumulation. The expression of endoglin was demonstrated in cultured human mesangial cells (HMC) by flow cytometry, Northern blot, reverse transcriptase polymerase chain reaction (RT-PCR), and Western blot analyses. TGF-beta upregulated not only the expression of endoglin, but also that of TGF-beta itself. TGF-beta receptor type II, collagen I, collagen IV, and fibronectin. To study the role of endoglin in TGF-beta responses, transfectant fibroblasts overexpressing endoglin were analyzed. Untreated and TGF-beta-treated endoglin cells showed significantly lower levels of collagens than those in control cells, indicating that endoglin negatively regulates ECM levels of collagens. These findings may have important implications in the pathological states associated with renal fibrosis. (C) 2002 Elsevier Science B.V. All rights reserved.
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收藏
页码：36 / 44
页数：9
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