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Louisiana State University Health Sciences Center in Shreveport
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Papers by Yuko miwa
Journal of the American Society of Nephrology, 2009
E-selectin and its ligands are essential for extravasation of leukocytes in inflammation. Here, w... more 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 Ϫ/Ϫ) 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 Ϫ/Ϫ 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 Ϫ/Ϫ 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 Ϫ/Ϫ neutrophils exhibited reduced E-selectin-dependent adherence to human umbilical vein endothelial cells in vitro. Injection of labeled neutrophils into mice showed that Bsg Ϫ/Ϫ neutrophils were less readily recruited to the kidney after renal ischemia/ reperfusion than Bsg ϩ/ϩ 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.
Journal of the American Society of Nephrology, 2009
E-selectin and its ligands are essential for extravasation of leukocytes in inflammation. Here, w... more 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 Ϫ/Ϫ) 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 Ϫ/Ϫ 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 Ϫ/Ϫ 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 Ϫ/Ϫ neutrophils exhibited reduced E-selectin-dependent adherence to human umbilical vein endothelial cells in vitro. Injection of labeled neutrophils into mice showed that Bsg Ϫ/Ϫ neutrophils were less readily recruited to the kidney after renal ischemia/ reperfusion than Bsg ϩ/ϩ 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.