Details

Autor(en) / Beteiligte

• KATO, Noritoshi
• YUZAWA, Yukio
• KOSUGI, Tomoki
• HOBO, Akinori
• SATO, Waichi
• MIWA, Yuko
• SAKAMOTO, Kazuma
• MATSUO, Seiichi
• KADOMATSU, Kenji

Titel

The E-Selectin Ligand Basigin/CD147 Is Responsible for Neutrophil Recruitment in Renal Ischemia/ Reperfusion

Ist Teil von

• Journal of the American Society of Nephrology, 2009-07, Vol.20 (7), p.1565-1576

Ort / Verlag

Washington, DC: American Society of Nephrology

Erscheinungsjahr

2009

Quelle

MEDLINE

Beschreibungen/Notizen

• E-selectin and its ligands are essential for extravasation of leukocytes in inflammation. Here, we report that basigin (Bsg)/CD147 is a ligand for E-selectin that promotes renal inflammation in ischemia/reperfusion. Compared with wild-type mice, Bsg-deficient (Bsg(-/-)) mice demonstrated striking suppression of neutrophil infiltration in the kidney after renal ischemia/reperfusion. Although E-selectin expression increased similarly between the two genotypes, Bsg(-/-) mice exhibited less renal damage, suggesting that Bsg on neutrophils contribute to renal injury in this model. Neutrophils expressed Bsg with N-linked polylactosamine chains and Bsg(-)(/)(-) neutrophils showed reduced binding to E-selectin. Bsg isolated from HL-60 cells bound to E-selectin, and tunicamycin treatment to abolish N-linked glycans from Bsg abrogated this binding. Furthermore, Bsg(-)(/)(-) neutrophils exhibited reduced E-selectin-dependent adherence to human umbilical vein endothelial cells in vitro. Injection of labeled neutrophils into mice showed that Bsg(-)(/)(-) neutrophils were less readily recruited to the kidney after renal ischemia/reperfusion than Bsg(+/+) neutrophils, regardless of the recipient's genotype. Taken together, these results indicate that Bsg is a physiologic ligand for E-selectin that plays a critical role in the renal damage induced by ischemia/reperfusion.