Expression of macrophage metalloelastase (MMP-12) in podocytes of hereditary nephrotic mice (ICGN strain).

The Institute for Cancer Research (ICR)-derived glomerulonephritis (ICGN) mouse is a good model for renal fibrosis. In the glomeruli and tubulointerstitium of ICGN mouse kidneys, the components of the extracellular matrix (ECM) accumulated, and matrix metalloproteinases (MMPs) participated in this process. To clarify the mechanism of renal fibrosis, we investigated the expression and localization of macrophage metalloelastase (MMP-12), whose functions in kidney diseases are not fully understood, and its regulatory molecules, monocyte chemoattractive protein-1 (MCP-1) and CC chemokine receptor 2 (CCR2), in the kidneys of ICGN mice by RT-PCR, Western blotting and immunohistochemical staining, respectively.

Immunochemical characteristics of a novel cell death receptor and a decoy receptor on granulosa cells of porcine ovarian follicles.

Previously, we prepared an IgM monoclonal antibody(PFG-1) which specifically recognized a cell-membraneglycoprotein (PFG-1 antigen; 55 kD, pI 5.9),immunohistochemically reacted with granulosa cells ofhealthy follicles but not of atretic follicles, andinduced granulosa cell apoptosis. In the presentstudy, an IgM monoclonal antibody (PFG-3) capable ofinducing granulosa cell apoptosis and an IgGmonoclonal antibody (PFG-4) not capable of inducingapoptosis were produced against granulosa cellsprepared from healthy antral follicles of porcineovaries.

Changes in the localization of type I, III and IV collagen mRNAs in the kidneys of hereditary nephritic (ICGN) mice with renal fibrosis.

Renal fibrotic change, extreme accumulation of extracellular matrix (ECM) components in glomeruli and tubulointerstitum, is one of the characteristic features of ICR-derived glomerulonephritis (ICGN) mice. Decreased degradation of ECMs by matrixmetalloproteinases was demonstrated in kidneys of ICGN mice. To determine the balance between production and degradation of ECMs in kidneys of ICGN mice, we examined expression of mRNAs of ECMs in those.

Down-regulation of connective tissue growth factor and type I collagen mRNA expression by connective tissue growth factor antisense oligonucleotide during experimental liver fibrosis.

Transforming growth factor (TGF)-beta 1 is a major mediator of liver fibrosis. Connective tissue growth factor (CTGF) mediates TGF-beta 1 pro-fibrogenic effects in vitro, but its in vivo role is unknown. Both TGF-beta 1 and CTGF are overexpressed in hepatic stellate cells during liver fibrosis.