作者: Y. Nishizawa , F. Fukai , Y. Natori , R. Kato , S. Tanuma
关键词:
摘要: We previously showed that in passive Heymann nephritis (PHN) rats, a large quantity of fibronectin (FN) fragments containing the central cell-binding (CCB) domain and adjacent domains are generated kidney excreted into urine (Nishizawa et al., Biol Pharm Bull 1998; 21: 429–433). To ascertain whether FN could affect progression PHN, we investigated effect 150 K fragment CCB carboxyl-terminal heparin-binding (Hep 2) on cultured rat mesangial cells. When cells FN-coated plates were exposed to fragment, some detached from substrate then underwent apoptosis as judged by nuclear DNA fragmentations. The competitively inhibited cell adhesion dose-dependent manner. Furthermore, gelatinzymography conditioned medium induced and/or poteintiated extracellular matrix (ECM)-degrading proteinases including metalloproteinases (MMPs) These results indicate may elicit disrupting through two distinct ways: inhibition ECM-degradation fragment-induced MMPs. Thus, kidneys PHN rats be involved evolution renal injury.