Open AccessFibrosis and matrix metalloproteinases in rat renal allografts
Author(s) -
Inkinen Kaija A.,
Soots Anu P.,
Krogerus Leena A.,
Lautenschlager Irmeli T.,
Ahonen Juhani P.
Publication year - 2005
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/j.1432-2277.2004.00053.x
Subject(s) - matrix metalloproteinase , chronic allograft nephropathy , medicine , in situ hybridization , zymography , pathology , fibrosis , transplantation , kidney , gene expression , messenger rna , gelatinase a , nephropathy , kidney transplantation , gene , biology , endocrinology , biochemistry , diabetes mellitus
Summary The temporal activity and gene expression of matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinase (TIMP) were investigated in a rat model of chronic allograft nephropathy. Gelatinolytic activity of MMP‐2 and ‐9 were demonstrated by zymography, and MMP‐2,‐9 and TIMP‐3 mRNA by in situ hybridization. The generation of fibrosis was determined as total collagen content/DNA. Significantly more latent and active MMP‐2, as well as latent MMP‐9, were seen in allografts than in autografts. Intense MMP‐2 mRNA expression was demonstrated in the allografts during the first 20 days after transplantation, located mainly in the interstitium of the kidney. In addition, some tubular cells expressed MMP‐2 mRNA. After day 20, MMP‐2 gene expression was faint. MMP‐9 mRNA expression in allografts was located mainly in the glomerulus. TIMP‐3 mRNA expression was downregulated in allografts. MMP‐2, MMP‐9 and TIMP‐3 seem to play a critical role in the development of fibrosis in the renal allograft.