Inhibitory effects of C‑type natriuretic peptide on the differentiation of cardiac fibroblasts, and secretion of monocyte chemoattractant protein‑1 and plasminogen activator inhibitor‑1

Li,Zhi‑Qiang; Liu,Ying‑Long; Li,Gang; Li,Bin; Liu,Yang; Li,Xiao‑Feng; Liu,Ai‑Jun

doi:10.3892/mmr.2014.2763

Inhibitory effects of C‑type natriuretic peptide on the differentiation of cardiac fibroblasts, and secretion of monocyte chemoattractant protein‑1 and plasminogen activator inhibitor‑1

Authors:
- Zhi‑Qiang Li
- Ying‑Long Liu
- Gang Li
- Bin Li
- Yang Liu
- Xiao‑Feng Li
- Ai‑Jun Liu
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Affiliations: Department of Pediatric Cardiac Surgery Center, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, P.R. China
Published online on: October 23, 2014 https://doi.org/10.3892/mmr.2014.2763
Pages: 159-165
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

The present study aimed to investigate the effect of C‑type natriuretic peptide (CNP) on the function of cardiac fibroblasts (CFs). Western blotting was used to investigate the expression of myofibroblast marker proteins: α‑smooth muscle actin (α‑SMA), extra domain‑A fibronectin, collagen I and collagen III, and the activity of extracellular signal‑regulated kinase 1/2 (ERK1/2). Immunofluorescence was used to examine the morphological changes; a transwell assay was used to analyze migration, and reverse transcription‑quantitative polymerase chain reaction and ELISA were employed to determine the mRNA expression and protein secretion of monocyte chemoattractant protein‑1 (MCP‑1) and plasminogen activator inhibitor‑1 (PAI‑1). The results demonstrated that CNP significantly reduced the protein expression of α‑SMA, fibronectin, collagen I and collagen III, and suppressed the migratory ability of CFs. Additionally, the mRNA and protein expression of MCP‑1 and PAI‑1 was inhibited under the CNP treatment; and this effect was mediated by the inhibition of the ERK1/2 activity. In conclusion, CNP inhibited cardiac fibroblast differentiation and migration, and reduced the secretion of MCP‑1 and PAI‑1, which demonstrates novel mechanisms to explain the antifibrotic effect of CNP.

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