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  4. Aldosterone induces tissue inhibitor of metalloproteinases-1 expression and further contributes to collagen accumulation: From clinical to bench studies
 
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Aldosterone induces tissue inhibitor of metalloproteinases-1 expression and further contributes to collagen accumulation: From clinical to bench studies

Journal
Hypertension
Journal Volume
67
Journal Issue
6
Pages
1309-1320
Date Issued
2016
Author(s)
CHI-SHENG HUNG  
Chou C.-H.
CHE-WEI LIAO  
Lin Y.-T.
Wu X.-M.
Chang Y.-Y.
YING-HSIEN CHEN  
VIN-CENT WU  
MING-JAI SU  
YI-LWUN HO  
MING-FONG CHEN  
YEN-HUNG LIN  
KWAN-DUN WU  
DOI
10.1161/HYPERTENSIONAHA.115.06768
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84968608604&doi=10.1161%2fHYPERTENSIONAHA.115.06768&partnerID=40&md5=df202de1595dc5b3ab2d1ca1b2fc0b36
https://scholars.lib.ntu.edu.tw/handle/123456789/515052
Abstract
Aldosterone induces myocardial fibrosis. Tissue inhibitor of metalloproteinases-1 (TIMP-1) is a key factor of myocardial fibrosis. This study tested the hypothesis that aldosterone induces TIMP-1 expression and contributes to the fibrotic process. We prospectively enrolled 54 patients with primary aldosteronism, and measured plasma TIMP-1 and echocardiographic parameters. In the cell study, we investigated the possible molecular mechanism by which aldosterone induces TIMP-1 secretion and the effects on collagen accumulation. In the animal study, we measured serum TIMP-1 levels, cardiac TIMP-1 levels, and cardiac structure in an aldosterone infusion mouse model using implantation of aldosterone pellets. In patients with primary aldosteronism, plasma TIMP-1 was correlated with 24-hour urinary aldosterone, left ventricular mass, and impairment of left ventricular diastolic function. In human cardiac fibroblasts, TIMP-1 protein and mRNA expressions were significantly increased by aldosterone through the glucocorticoid receptor/PI3K/Akt/nuclear factor-κB pathway. TIMP-1 small-interfering RNA significantly reduced aldosterone-induced collagen accumulation, and aldosterone did not alter the levels of collagen1a1 or matrix metalloproteinase-1 mRNA. The aldosterone-induced TIMP-1 expression was inversely related to matrix metalloproteinase-1 activity. Furthermore, in the animal model, the serum and cardiac levels of TIMP-1 were significantly elevated in the mice that received aldosterone infusion. This elevation was blocked by RU-486 but not by eplerenone, suggesting that the effect was through glucocorticoid receptors. In a long-term aldosterone infusion model, serum TIMP-1 was associated with serum aldosterone level, cardiac structure, and fibrosis. In conclusion, aldosterone induced TIMP-1 expression in vivo and in vitro. This increased TIMP-1 expression resulted in enhanced collagen accumulation via the suppression of matrix metalloproteinase-1 activity. ? 2016 American Heart Association, Inc.
SDGs

[SDGs]SDG3

Publisher
Lippincott Williams and Wilkins
Type
journal article

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