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- W13806405 abstract "Abstract Renal ischemia reperfusion injury (IRI) is a major cause of acute injury in both native and transplanted kidneys. This type of kidney injury is considered an antigen-independent inflammatory condition that involves multiple factors leading to tubular and endothelial dysfunction. We have recently found that NK cells induce apoptosis in tubular epithelial cells (TEC) and contribute to renal IRI. Kidney can express osteopontin (OPN) during injury. Therefore we examined the role OPN in NK cell function and kidney IRI. We have found that TEC expressed high levels of OPN in vitro and in vivo after injury. Kidneys in OPN-/- mice had less severity of IRI compared to wild-type mice (P<0.05). Interestingly, recombinant OPN could activate NK cells that express high levels of perforin and granzyme and could mediate TEC apoptotic death. Importantly, we have found that NK cell migrate towards OPN protein as well as OPN-producing TEC in the transwell assay. Whereas, less NK cell migration was seen towards OPN-/- TEC (P<0.01). Further more, Kidneys in OPN-/- mice had less NK cell infiltration after IRI compared to WT mice (P<0.02). Taken together, our study results support a previously unrecognized role for TEC expression of OPN in NK cell-mediated kidney injury. TEC expression of OPN promotes early kidney inflammatory and IRI, and limiting OPN expression may improve kidney function and graft survival." @default.
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- W13806405 date "2009-04-01" @default.
- W13806405 modified "2023-09-28" @default.
- W13806405 title "OPN expression by epithelial tubular cells regulates NK cell-mediated kidney ischemia reperfusion injury (98.30)" @default.
- W13806405 doi "https://doi.org/10.4049/jimmunol.182.supp.98.30" @default.
- W13806405 hasPublicationYear "2009" @default.
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