The regulation of the extracellular matrix turnover in the experimental glomerulopathies.
Pathogenic mechanisms invoved in glomerulopathies were investigated on the passive form of accelerate model of nephrotoxic nephritis and puromycin aminonucleoside nephrosis. The aim of the present study was to examine the interaction of some cytokines produced by mononuclear leukocytes and mesangial cells in a regulation of synthesis and degradation of the extracellular matrix components and adhesion molecules expression. In acute stage of nephrotoxic nephritis and puromycin aminonucleoside nephrosis the mononuclear leukocyte infiltration into glomeruli was noted. Mononuclear leukocytes produce cytokines that control mesangial cells proliferation and extracellular matrix accumulation. In summary the current study showed a key role of mononuclear leukocytes in inflammation and extracellular matrix turnover. The absence of mononuclear leukocytes or their abundance induce the disturbance of extracellular matrix synthesis and progression factors in glomerulosclerosis.
D000818:Animals; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002455:Cell Division; D016207:Cytokines / Q000096:biosynthesis*; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D005920:Glomerular Mesangium / Q000166:cytology; D005921:Glomerulonephritis / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D007668:Kidney / Q000473:pathology* / Q000648:ultrastructure; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000166:cytology; D008297:Male; D008854:Microscopy, Electron; D009401:Nephrosis / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D016212:Transforming Growth Factor beta / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D015815:Cell Adhesion Molecules; D016207:Cytokines; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha