| Autor: |
Ac, Lane, Dw, Johnson, X-J, Zhang, L, Cuttle, Da, Willgoss, Cm, Winterford, Zh, Endre, GC., Gobé |
| Předmět: |
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| Zdroj: |
Nephrology; Oct2000, Vol. 5 Issue 3, pA101, 1p |
| Abstrakt: |
The presence of myofibroblasts (α-SMA antibody), macrophages (ED2 antibody), collagen deposition (Azan stain), tubulo-interstitial cell apoptosis (morphology and ISEL) or mitosis (³H-thymidine uptake), and expression of specific growth factors (immuno-localisation of TGF-β1, PDGF, IGF-I and -II) were studied in an established rat model of progressive renal fibrosis, to analyse for any temporal and spatial links amongst these factors. A renal papillotoxin was used to induce renal papillary necrosis and subsequent healing of this lesion was followed by development of focal tubulo-interstitial fibrosis that was studied at 2, 4, 8 and 12 weeks. A temporo-spatial correlation between tubulo-interstitial myofibroblasts (TIMs) and collagen deposition was verified. TIMs and macrophages were identified at all experimental times, but some fibrotic foci had only TIMs, emphasising their fibrogenic potential. TGF-β1 was detectable at all times within the fibrotic lesions, with TIMs having TGF-β1 expression, indicating a close link between the TIMs and the pro-fibrotic protein. PDGF-B, IGF-I and II were detected but had no apparent close link with progression of fibrosis. A high level of interstitial cell mitosis was measured in fibrotic lesions at 4 weeks. Apoptotic myofibroblasts (electron microscopy or ISEL plus α-SMA) had highest incidence in the small fibrotic lesions at 2 and 4 weeks compared with their incidence in larger established lesions at later times, indicating apoptotic deletion of myofibroblasts may have a role in controlling development of extensive renal fibrosis. Research supported by an ARC Small Grant and the AKF. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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