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C-type natriuretic peptide suppresses mesangial proliferation and matrix expression via a MMPs/TIMPs-independent pathway in vitro.

Authors
  • Huang, Bao Yu1
  • Hu, Peng1
  • Zhang, Dong Dong1
  • Jiang, Guang Mei1
  • Liu, Si Yan1
  • Xu, Yao1
  • Wu, Yang Fang1
  • Xia, Xun1
  • Wang, Ya2
  • 1 a Department of Pediatrics , The First Affiliated Hospital of Anhui Medical University , Hefei , PR China. , (China)
  • 2 b Anhui Provincial Children's Hospital , Hefei , PR China. , (China)
Type
Published Article
Journal
Journal of Receptors and Signal Transduction
Publisher
Informa UK (Taylor & Francis)
Publication Date
Aug 01, 2017
Volume
37
Issue
4
Pages
355–364
Identifiers
DOI: 10.1080/10799893.2017.1286674
PMID: 28554303
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

C-type natriuretic peptide (CNP) acts mainly in a local, paracrine fashion to regulate vascular tone and cell proliferation. Although several in vivo studies have demonstrated that CNP exerts an inhibitory effect on mesangial matrix generation, a limited number of reports exist about the anti-extracellular matrix (ECM) accumulation effect of CNP and its underlying mechanisms in mesangial cells (MCs) in vitro. In this study, human MCs were incubated in serum-containing medium in the absence or presence of CNP (0, 10 and 100 pM) for 24, 48 and 72 h, respectively. CNP administration significantly suppresses MCs proliferation and collagen (Col)-IV expression in a time- and dose-dependent manner. In addition, the study presented herein was designed as a first demonstration of the regulative effects of CNP on the metabolisms of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in MCs in vitro, and found that: (1) CNP administration significantly decreased the secretion and expression of MMP-2 and MMP-9 in the cultured MCs; (2) the secretion and expression of TIMP-1 progressively elevated after treatment with CNP for 24 and 48 h, whereas declined at later time point; (3) CNP expression was negatively correlated with MMP-2 and MMP-9 expression; (4) the balance of MMPs/TIMPs was shifted toward the reduction in MMP-2 and MMP-9 activity and/or the increment in TIMP-1 expression, which could not account for the down-regulation of Col-IV expression in CNP-treated MCs. In conclusion, CNP suppresses mesangial proliferation and ECM expression via a MMPs/TIMPs-independent pathway in vitro.

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