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

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

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)212-219
Number of pages8
JournalClinical and Experimental Nephrology
Issue number2
Publication statusPublished - Apr 2011


  • ICAM-1
  • Inflammation
  • Macrophage
  • TGF-β
  • Type IV collagen

ASJC Scopus subject areas

  • Physiology
  • Nephrology
  • Physiology (medical)


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