Endothelin-1 and endothelin B type receptor are induced in mesangial proliferative nephritis in the rat.
Endothelin-1 and endothelin B type receptor are induced in mesangial proliferative nephritis in the rat.
复制标题
大鼠系膜增生性肾炎中诱导内皮素-1 和内皮素 B 型受体。
DOI:
10.1038/ki.1995.413
复制
发表时间:
1995
影响因子:
19.6
通讯作者:
T. Masaki
中科院分区:
文献类型:
--
作者:
A. Yoshimura;S. Iwasaki;K. Inui;T. Ideura;S. Koshikawa;M. Yanagisawa;T. Masaki
We studied whether endothelin-1 (ET-1) and its receptor subtypes (ETAR, endothelin A type receptor; and ETBR, B type receptor) were up-regulated in the glomerulus of a rat model of mesangial proliferative glomerulonephritis induced by anti-thymocyte serum (anti-Thy-1 GN). A marked increase in preproET-1 mRNA could be demonstrated in glomerular RNA 3 and six days after disease induction (4.1- and 4.9-fold vs. day 0, respectively), corresponding to the time of mesangial cell proliferation, to the time of macrophage infiltration into glomeruli, and also to the time of increase in glomerular PDGF B-chain mRNA expression. The localization of ET-1 protein in the mesangial area and along the inner aspect of the glomerular capillary wall was also demonstrated by immunohistochemistry from day 3 and maximal at day 6. The major source of the cells expressing ET-1 in glomeruli appeared to be mesangial cells, glomerular endothelial cells and monocyte/macrophages. Furthermore, both gene and protein expression of ET-1 were associated with increased urinary excretion of ET-1. There was no increase in the plasma ET-1 immunoreactivity. Glomerular expression of ETBR mRNA increased in anti-Thy-1 GN (1.5-fold vs. day 0 at day 3 after disease induction, 3.6-fold at day 6 and 2.7-fold at day 10), but there was minimal change in ETAR mRNA expression. These results suggest that preproET-1 mRNA, which is induced in anti-Thy-1 GN, is linked primarily with ETBR mRNA expression.(ABSTRACT TRUNCATED AT 250 WORDS)
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DOI:
10.1152/ajprenal.1991.261.1.f117
发表时间:
1991
期刊:
The American journal of physiology
影响因子:
--
作者:
Marsden,PA;Dorfman,DM;Collins,T;Brenner,BM;Orkin,SH;Ballermann,BJ
通讯作者:
Ballermann,BJ
DOI:
--
发表时间:
1993
期刊:
The American journal of pathology
影响因子:
--
作者:
Floege,J;Johnson,RJ;Alpers,CE;Fatemi-Nainie,S;Richardson,CA;Gordon,K;Couser,WG
通讯作者:
Couser,WG
DOI:
--
发表时间:
1994
期刊:
The American journal of pathology
影响因子:
--
作者:
Takeda,M;Iwasaki,S;Hellings,SE;Yoshida,H;Homma,T;Kon,V
通讯作者:
Kon,V
DOI:
10.1172/jci114079
发表时间:
1989
期刊:
The Journal of clinical investigation
影响因子:
--
作者:
Kon,V;Yoshioka,T;Fogo,A;Ichikawa,I
通讯作者:
Ichikawa,I
影响因子:
19.6
作者:
A. Yoshimura;K. Gordon;C. Alpers;J. Floege;P. Pritzl;R. Ross;W. Couser;D. Bowen-Pope;Richard J. Johnson
通讯作者:
A. Yoshimura;K. Gordon;C. Alpers;J. Floege;P. Pritzl;R. Ross;W. Couser;D. Bowen-Pope;Richard J. Johnson