Matrix metalloproteinase 2 improves the transplanted adipocyte survival in mice.

Abstract:

BACKGROUND:Fat tissue is a common material for autologous transplantation in plastic and reconstructive surgery. Basic fibroblast growth factor (bFGF) ameliorates the fat graft survival. A transplantation model has shown the gene expression of matrix metalloproteinases (MMPs) to increase in adipocytes. The aim of this study is to investigate the role of MMPs in the amelioration of survival by bFGF. MATERIALS AND METHODS:3T3-L1 adipocytes were incubated with or without 10 microg mL(-1) bFGF for 8 h in the presence or absence of the MMP inhibitor GM6001, vascular endothelial growth factor (VEGF), MMP-2 or anti-bFGF antibody to study the effect of bFGF on MMP-2 mRNA expression, MMP-2 activity, fat accumulation or 2-deoxyglucose uptake. Collagen sheets containing l x l0(7) adipocytes with or without bFGF in the presence or absence of GM6001 were subcutaneously transplanted into mice, and the appearance, histology, mRNA expression and fat accumulation of the grafts were analysed 4 weeks after transplantation. RESULTS:The MMP-2 expression was drastically induced by bFGF among MMPs in 3T3-L1 adipocytes. MMP-2 accelerated fat accumulation, peroxisome proliferator-activated receptor gamma (PPAR gamma) mRNA expression, and glucose uptake to an extent similar to those induced by bFGF, respectively. The bFGF-induced increases were inhibited by the blocking of MMP-2. The transplantation of adipocytes into mice showed that bFGF ameliorates the appearance and fat accumulation, as well as mRNA expression in grafts. These effects were almost or partly inhibited by a MMP blockade. CONCLUSIONS:MMP-2 may be involved in the mechanism by which bFGF ameliorates the survival of fat grafts.

journal_name

Eur J Clin Invest

authors

Kuramochi D,Unoki H,Bujo H,Kubota Y,Jiang M,Rikihisa N,Udagawa A,Yoshimoto S,Ichinose M,Saito Y

doi

10.1111/j.1365-2362.2008.02023.x

subject

Has Abstract

pub_date

2008-10-01 00:00:00

pages

752-9

issue

10

eissn

0014-2972

issn

1365-2362

pii

ECI2023

journal_volume

38

pub_type

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