Expression profile of extracellular matrix and its regulatory proteins during the process of interstitial fibrosis after anti-glomerular basement membrane antibody-induced glomerular sclerosis in Sprague-Dawley rats
| Autor: | Eishin Yaoita, Yoshimasa Nakano, Katsutoshi Kawasaki, Masato Isome, Itaru Kihara, Laxman P. Adhikary, Tadashi Yamamoto |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Male
Pathology medicine.medical_specialty Kidney Cortex MMP2 Kidney Glomerulus urologic and male genital diseases Antibodies Basement Membrane Pathology and Forensic Medicine Rats Sprague-Dawley Extracellular matrix Fibrosis medicine Animals RNA Messenger Basement membrane Extracellular Matrix Proteins biology Glomerulosclerosis Focal Segmental urogenital system General Medicine medicine.disease female genital diseases and pregnancy complications Extracellular Matrix Rats Fibronectin Proteinuria medicine.anatomical_structure Tubulointerstitial fibrosis biology.protein Nephritis Immunostaining |
| Zdroj: | Pathology International. 49:716-725 |
| ISSN: | 1440-1827 1320-5463 |
| DOI: | 10.1046/j.1440-1827.1999.00939.x |
| Popis: | Anti-glomerular basement membrane (GBM) nephritis in Sprague-Dawley (SD) rats was characterized by development of marked glomerular sclerosis and tubulointerstitial fibrosis. To elucidate sequential change of the glomerular sclerosis and tubulointerstitial fibrosis, accumulation and mRNA expression of extracellular matrix (ECM) components and transforming growth factor (TGF)-beta were examined in the glomerulus and cortex during the disease course by histology, immunostaining and ribonuclease protection assay. Mild proliferative and degenerative lesions appeared in the glomeruli by day 15 after anti-GBM antibody binding to GBM and progressed to glomerular sclerotic lesion thereafter. Conversely, interstitial change was first recognized by infiltration of mononuclear cells after day 20, followed by marked accumulation of ECM and tubular degeneration. The interstitial fibrosis was induced without apparent binding of anti-GBM antibody to tubular basement membrane. Accumulation of fibronectin, collagen type I and type IV was noted in the interstitium by immunofluorescence microscopy in association with enhanced expression of mRNA for these ECM components and their regulatory molecules such as matrix metalloproteinase (MMP2), tissue inhibitor of metalloproteinase (TIMP)-1 and TGF-beta1 both in glomeruli and cortex. The glomerular expression of these mRNA increased apparently by day 15 and reached a plateau or a peak at day 20. The expression of the same mRNA increased gradually from day 15 to day 29 in the cortex. These observations show that interstitial fibrosis follows glomerular sclerosis after anti-GBM antibody injection in SD rats, suggesting that at least a part of the mechanism for ECM accumulation in the glomerulus and interstitium is essentially the same in terms of composition of ECM and expression of its regulatory molecules. |
| Databáze: | OpenAIRE |
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