Intercellular adhesion molecule-1 plays a critical role in glomerulosclerosis after subtotal nephrectomy.

Kido, Yuichi; Ogawa, Daisuke; Shikata, Kenichi; Sasaki, Motofumi; Nagase, Ryo; Okada, Shinichi; Usui Kataoka, Hitomi; Wada, Jun; Makino, Hirofumi

Background: Hyperfiltration in the glomeruli have been considered to be an important cause of glomerular injury; however, the role of intercellular adhesion molecule (ICAM)-1 in the pathogenesis of glomerulosclerosis is not known. Methods: To elucidate the effects of ICAM-1 depletion on hyperfiltration-induced glomerular disorder, we used subtotally nephrectomized ICAM-1 and ICAM-1 mice. We evaluated macrophage infiltration, mesangial matrix expansion, transforming growth factor (TGF)-β and type IV collagen accumulation in glomeruli. Results: Macrophage infiltration into the glomeruli and mesangial matrix expansion coincident with increased expression of both ICAM-1 and TGF-β, and accumulation of type IV collagen were ameliorated in subtotally nephrectomized ICAM-1 mice compared to ICAM-1 mice. ICAM-1 depletion significantly reduced hyperfiltration-induced glomerular injury after renal ablation. Conclusions: Our present findings suggest that glomerular hyperfiltration is the leading cause of glomerulosclerosis, and it is mediated, at least in part, by ICAM-1 expression and macrophage infiltration.

CELL adhesion molecules; KIDNEY glomerulus; LABORATORY mice; TRANSFORMING growth factors; COLLAGEN; MACROPHAGES; INFLAMMATION; GENE expression

Clinical & Experimental Nephrology, 2011, Vol 15, Issue 2, p212

1342-1751

Academic Journal

10.1007/s10157-010-0388-7