Adenosine mediates transforming growth factor-beta 1 release in kidney glomeruli of diabetic rats

被引:47
作者
Roa, H. [1 ]
Gajardo, C. [1 ]
Troncoso, E. [1 ]
Fuentealba, V. [1 ]
Escudero, C. [2 ,3 ]
Yanez, A. [1 ]
Sobrevia, L. [2 ,3 ]
Pastor-Anglada, M. [4 ,5 ]
Quezada, C. [1 ]
San Martin, R. [1 ]
机构
[1] Univ Austral Chile, Lab Patol Mol, Inst Bioquim, Fac Ciencias, Valdivia, Chile
[2] Pontificia Univ Catolica Chile, Fac Med, Sch Med, Dept Obstet & Gynaecol,Med Res Ctr CIM,CMPL, Santiago, Chile
[3] Pontificia Univ Catolica Chile, Fac Med, Sch Med, Dept Obstet & Gynaecol,Med Res Ctr CIM,PRL, Santiago, Chile
[4] Univ Barcelona, Inst Biomed, Dept Bioquim & Biol Mol, E-08007 Barcelona, Spain
[5] CIBER EHD, Barcelona, Spain
来源
FEBS LETTERS | 2009年 / 583卷 / 19期
关键词
Adenosine receptor; Transforming growth factor-beta 1; Diabetic nephropathy; Glomerulus; EQUILIBRATIVE NUCLEOSIDE TRANSPORTER; MESANGIAL CELLS; EXPRESSION LEVEL; TGF-BETA; PROTEIN-KINASE; HIGH GLUCOSE; NEPHROPATHY; RECEPTOR; STIMULATION; INSULIN;
D O I
10.1016/j.febslet.2009.09.003
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
Up regulation of the transforming growth factor-beta 1 (TGF-beta 1) axis has been recognized as a pathogenic event for progression of glomerulosclerosis in diabetic nephropathy. We demonstrate that glomeruli isolated from diabetic rats accumulate up to sixfold more extracellular adenosine than normal rats. Both decreased nucleoside uptake activity by the equilibrative nucleoside transporter 1 and increased AMP hydrolysis contribute to raise extracellular adenosine. Ex vivo assays indicate that activation of the low affinity adenosine A(2B) receptor subtype (A(2B)AR) mediates TGF-beta 1 release from glomeruli of diabetic rats, a pathogenic event that could support progression of glomerulopathy when the bioavailability of adenosine is increased. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3192 / 3198
页数:7
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