TY - JOUR
T1 - Intercellular adhesion molecule-1 plays a critical role in glomerulosclerosis after subtotal nephrectomy
AU - Kido, Yuichi
AU - Ogawa, Daisuke
AU - Shikata, Kenichi
AU - Sasaki, Motofumi
AU - Nagase, Ryo
AU - Okada, Shinichi
AU - Usui Kataoka, Hitomi
AU - Wada, Jun
AU - Makino, Hirofumi
PY - 2011/4
Y1 - 2011/4
N2 - 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.
AB - 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.
KW - ICAM-1
KW - Inflammation
KW - Macrophage
KW - TGF-β
KW - Type IV collagen
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U2 - 10.1007/s10157-010-0388-7
DO - 10.1007/s10157-010-0388-7
M3 - Article
C2 - 21181224
AN - SCOPUS:79959222531
VL - 15
SP - 212
EP - 219
JO - Clinical and Experimental Nephrology
JF - Clinical and Experimental Nephrology
SN - 1342-1751
IS - 2
ER -