Document Detail


Macrophage matrix metalloproteinase-9 mediates epithelial-mesenchymal transition in vitro in murine renal tubular cells.
MedLine Citation:
PMID:  20075196     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
As a rich source of pro-fibrogenic growth factors and matrix metalloproteinases (MMPs), macrophages are well-placed to play an important role in renal fibrosis. However, the exact underlying mechanisms and the extent of macrophage involvement are unclear. Tubular cell epithelial-mesenchymal transition (EMT) is an important contributor to renal fibrosis and MMPs to induction of tubular cell EMT. The aim of this study was to investigate the contribution of macrophages and MMPs to induction of tubular cell EMT. The murine C1.1 tubular epithelial cell line and primary tubular epithelial cells were cultured in activated macrophage-conditioned medium (AMCM) derived from lipopolysaccharide-activated J774 macrophages. MMP-9, but not MMP-2 activity was detected in AMCM. AMCM-induced tubular cell EMT in C1.1 cells was inhibited by broad-spectrum MMP inhibitor (GM6001), MMP-2/9 inhibitor, and in AMCM after MMP-9 removal by monoclonal Ab against MMP-9. AMCM-induced EMT in primary tubular epithelial cells was inhibited by MMP-2/9 inhibitor. MMP-9 induced tubular cell EMT in both C1.1 cells and primary tubular epithelial cells. Furthermore, MMP-9 induced tubular cell EMT in C1.1 cells to an extent similar to transforming growth factor-beta. Transforming growth factor-beta-induced tubular cell EMT in C1.1 cells was inhibited by MMP-2/9 inhibitor. Our in vitro study provides evidence that MMPs, specifically MMP-9, secreted by effector macrophages can induce tubular cell EMT and thereby contribute to renal fibrosis.
Authors:
Thian Kui Tan; Guoping Zheng; Tzu-Ting Hsu; Ying Wang; Vincent W S Lee; Xinrui Tian; Yiping Wang; Qi Cao; Ya Wang; David C H Harris
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-14
Journal Detail:
Title:  The American journal of pathology     Volume:  176     ISSN:  1525-2191     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-10     Completed Date:  2010-06-07     Revised Date:  2011-07-25    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1256-70     Citation Subset:  AIM; IM    
Affiliation:
Centre for Transplantation and Renal Research, the University of Sydney at Westmead Millennium Institute, Sydney, NSW 2145 Australia. ttan4526@mail.usyd.edu.au
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism
Animals
Cell Line
Cells, Cultured
Culture Media, Conditioned / pharmacology
Dipeptides / pharmacology
Epithelial Cells / drug effects,  enzymology*,  pathology*
Epithelium / enzymology*,  pathology
Fibrosis / metabolism
Intercellular Signaling Peptides and Proteins / metabolism
Kidney Tubules / pathology*
Lipopolysaccharides / pharmacology
Macrophage Activation / drug effects
Macrophages / drug effects,  enzymology*,  pathology
Matrix Metalloproteinase 2 / antagonists & inhibitors,  metabolism
Matrix Metalloproteinase 9 / antagonists & inhibitors,  metabolism*
Mesoderm / drug effects,  enzymology*,  pathology
Mice
Mice, Inbred BALB C
Phenotype
Protein Transport / drug effects
Recombinant Proteins / pharmacology
Ureteral Obstruction / enzymology,  pathology
Chemical
Reg. No./Substance:
0/Actins; 0/Culture Media, Conditioned; 0/Dipeptides; 0/GM 6001; 0/Intercellular Signaling Peptides and Proteins; 0/Lipopolysaccharides; 0/Recombinant Proteins; EC 3.4.24.24/Matrix Metalloproteinase 2; EC 3.4.24.35/Matrix Metalloproteinase 9
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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