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

Kato, Noritoshi; Yuzawa, Yukio; Kosugi, Tomoki; Hobo, Akinori; Sato, Waichi; Miwa, Yuko; Sakamoto, Kazunari; Matsuo, Seiichi; Kadomatsu, Kenji

doi:10.1681/asn.2008090957

Cited by 94 publications

(97 citation statements)

References 50 publications

(49 reference statements)

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“…It is known that macrophages express Bsg, and that Bsg could be a ligand for E-selectin. 27,34 We also confirmed that Bsg on THP-1, the human monocytic cell line, bound to E-selectin (data not shown). Consider- ing that E-selectin expression was induced to similar degrees in both genotypes, it is likely that the difference in macrophage infiltration between Bsg ϩ/ϩ and Bsg Ϫ/Ϫ mice is due to the presence of Bsg on macrophages.…”

Section: Discussionsupporting

confidence: 63%

“…44 However, little information about E-selectin is available. Because Bsg acts as an E-selectin ligand on inflammatory cells, 34 we next examined E-selectin expression in the kidney. We found that E-selectin expression was upregulated in the kidney after UUO surgery, but the expression levels were comparable between the genotypes ( Figure 2C).…”

Section: Macrophage Infiltration Is Lower In Bsg ϫ/ϫ Micementioning

confidence: 99%

“…[31][32][33] Most recently, we also found that Bsg is an E-selectin ligand and is involved in renal ischemia/reperfusion injury. 34 In this study, we focused on Bsg functions in renal fibrosis induced by unilateral ureteral obstruction (UUO). Bsg orchestrates renal fibrosis formation through MMPs, hyaluronan production, and macrophage infiltration.…”

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confidence: 99%

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Basigin/CD147 Promotes Renal Fibrosis after Unilateral Ureteral Obstruction

Kato

Kosugi

Sato

et al. 2011

The American Journal of Pathology

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Regardless of their primary causes, progressive renal fibrosis and tubular atrophy are the main predictors of progression to end-stage renal disease. Basigin/ CD147 is a multifunctional molecule-it induces matrix metalloproteinases and hyaluronan, for example-and has been implicated in organ fibrosis. However, the relationship between basigin and organ fibrosis has been poorly studied. We investigated basigin's role in renal fibrosis using a unilateral ureteral obstruction model. Basigin-deficient mice (Bsg ؊/؊ ) demonstrated significantly less fibrosis after surgery than Bsg ؉/؉ mice. Fewer macrophages had infiltrated in Bsg ؊/؊ kidneys. Consistent with these in vivo data, primary cultured tubular epithelial cells from Bsg ؊/؊ mice produced less matrix metalloproteinase and exhibited less motility on stimulation with transforming growth factor ␤. Furthermore, Bsg ؊/؊ embryonic fibro blasts produced less hyaluronan and ␣-smooth muscle actin after transforming growth factor ␤ stimulation. Together, these results demonstrate for the first time that basigin is a key regulator of renal fibrosis. Basigin could be a candidate target molecule for the prevention of organ fibrosis.

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Section: Discussionsupporting

confidence: 63%

Section: Macrophage Infiltration Is Lower In Bsg ϫ/ϫ Micementioning

confidence: 99%

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Basigin/CD147 Promotes Renal Fibrosis after Unilateral Ureteral Obstruction

Kato

Kosugi

Sato

et al. 2011

The American Journal of Pathology

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“…The respiratory syncytial virus receptor, CX3CR1 (48,49), is found on intestinal macrophages, whereas CD81, an entry factor for hepatitis C virus, is also found on macrophages (50,51). Finally, it is evident from previous studies that Fc-FcγR-mediated cellular immunity plays a major role in mounting an effective protective response toward bacterial pathogens (52,53). Even in those circumstances, it is possible that a molecular bridge between the pathogen and the effector cell may enhance cell-mediated immunity.…”

Section: Discussionmentioning

confidence: 97%

Optimal activation of Fc-mediated effector functions by influenza virus hemagglutinin antibodies requires two points of contact

Leon

Mullarkey

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

107

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Influenza virus strain-specific monoclonal antibodies (mAbs) provide protection independent of Fc gamma receptor (FcγR) engagement. In contrast, optimal in vivo protection achieved by broadly reactive mAbs requires Fc-FcγR engagement. Most strain-specific mAbs target the head domain of the viral hemagglutinin (HA), whereas broadly reactive mAbs typically recognize epitopes within the HA stalk. This observation has led to questions regarding the mechanism regulating the activation of Fc-dependent effector functions by broadly reactive antibodies. To dissect the molecular mechanism responsible for this dichotomy, we inserted the FLAG epitope into discrete locations on HAs. By characterizing the interactions of several FLAG-tagged HAs with a FLAG-specific antibody, we show that in addition to Fc-FcγR engagement mediated by the FLAG-specific antibody, a second intermolecular bridge between the receptor-binding region of the HA and sialic acid on effector cells is required for optimal activation. Inhibition of this second molecular bridge, through the use of an F(ab′) 2 or the mutation of the sialic acid-binding site, renders the Fc-FcγR interaction unable to optimally activate effector cells. Our findings indicate that broadly reactive mAbs require two molecular contacts to possibly stabilize the immunologic synapse and potently induce antibody-dependent cell-mediated antiviral responses: (i) the interaction between the Fc of a mAb bound to HA with the FcγR of the effector cell and (ii) the interaction between the HA and its sialic acid receptor on the effector cell. This concept might be broadly applicable for protective antibody responses to viral pathogens that have suitable receptors on effector cells. hemagglutinin | influenza virus | antibody-dependent cell-mediated immunity | broadly reactive antibodies | Fcγ receptor

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“…Proteinaceous casts, tubular necrosis, and medullary congestion are established histologic features of ischemic AKI. 1,2,18,19 Histologic analyses revealed that Klf4 deletion significantly exacerbated the formation of proteinaceous casts and tubular necrosis and the degree of medullary congestion in response to I/R injury ( Figure 3). These results suggest that endothelial Klf4 plays a protective role in ischemic AKI.…”

Section: Endothelial Klf4 Deletion Exacerbated Renal I/r Injurymentioning

confidence: 99%

Endothelial Krüppel-Like Factor 4 Mediates the Protective Effect of Statins against Ischemic AKI

Yoshida

Yamashita

Iwai

et al. 2015

JASN

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Endothelial cells participate in the pathophysiology of ischemic AKI by increasing the expression of cell adhesion molecules and by recruiting inflammatory cells. We previously showed that endothelial Krüppel-like factor 4 (Klf4) regulates vascular cell adhesion molecule 1 (Vcam1) expression and neointimal formation after carotid injury. In this study, we determined whether endothelial Klf4 is involved in ischemic AKI using endothelial Klf4 conditional knockout (Klf4 cKO) mice generated by breeding Tek-Cre mice and Klf4 floxed mice. Klf4 cKO mice were phenotypically normal before surgery. However, after renal ischemia-reperfusion injury, Klf4 cKO mice exhibited elevated serum levels of urea nitrogen and creatinine and aggravated renal histology compared with those of Klf4 floxed controls. Moreover, Klf4 cKO mice exhibited enhanced accumulation of neutrophils and lymphocytes and elevated expression of cell adhesion molecules, including Vcam1 and Icam1, in injured kidneys. Notably, statins ameliorated renal ischemia-reperfusion injury in control mice but not in Klf4 cKO mice. Mechanistic analyses in cultured endothelial cells revealed that statins increased KLF4 expression and that KLF4 mediated the suppressive effect of statins on TNFa-induced VCAM1 expression by reducing NF-kB binding to the VCAM1 promoter. These results provide evidence that endothelial Klf4 is renoprotective and mediates statin-induced protection against ischemic AKI by regulating the expression of cell adhesion molecules and concomitant recruitment of inflammatory cells.

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

Cited by 94 publications

References 50 publications

Basigin/CD147 Promotes Renal Fibrosis after Unilateral Ureteral Obstruction

Basigin/CD147 Promotes Renal Fibrosis after Unilateral Ureteral Obstruction

Optimal activation of Fc-mediated effector functions by influenza virus hemagglutinin antibodies requires two points of contact

Endothelial Krüppel-Like Factor 4 Mediates the Protective Effect of Statins against Ischemic AKI

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