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Human CC chemokine CCL23 enhances expression of matrix metalloproteinase-2 and invasion of vascular endothelial cells.

Abstract：

:Human CCL23 (also known as CKbeta8, MPIF-1, or MIP-3) has been recently reported to induce endothelial cell migration and tube formation via CCR1. Matrix metalloproteinases (MMPs) are involved in the degradation of the extracellular matrix and also appear to play critical roles in angiogenesis. In the present study, we have demonstrated that CCL23 enhances the expression of MMP-2 mRNA and protein levels in endothelial cells in a dose-dependent manner, but has no effect on the expression levels of MMP-9, TIMP-1, TIMP-2, and MT1-MMP. CCL23 was shown to dose-dependently activate the expression of the MMP-2/Luc reporter gene, thereby indicating that it stimulates the transcription of the MMP-2 gene. Vascular endothelial cells, when exposed to CCL23, showed a marked ability to invade through a 3D Matrigel. This increase in invasion was also correlated with enhancements in the expression and activity of MMP-2. Neutralization with anti-CCL23 and anti-CCR1 antibodies, as well as the heat-induced inactivation of CCL23, resulted in a blockage of the CCL23-activated invasion, indicating that the invasion of HUVECs was induced by CCL23 specifically. Furthermore, we showed that the CCL23-induced invasion was inhibited by MMP inhibitors such as GM6001 and a specific MMP-2 Inhibitor I. Our results indicate that CCL23 may play a direct role in angiogenesis, via the upregulation of MMP-2 expression.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Son KN,Hwang J,Kwon BS,Kim J

doi

10.1016/j.bbrc.2005.12.037

subject

Has Abstract

pub_date

2006-02-10 00:00:00

pages

498-504

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(05)02800-7

journal_volume

340

pub_type

杂志文章

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