{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T13:32:27Z","timestamp":1762176747433},"reference-count":53,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2014,9,15]]},"abstract":"<jats:p> Acute kidney injury (AKI) increases the risk of morbidity and mortality after major surgery and transplantation. We investigated the effect of PKC-\u03b5 deficiency on AKI and ischemic allograft damage after kidney transplantation. PKC-\u03b5-deficient and wild type (WT) control mice were subjected to 35 min of renal pedicle clamping to induce AKI. PKC-\u03b5 deficiency was associated with a marked improvement in survival and an attenuated loss of kidney function. Furthermore, functional MRI experiments revealed better renal perfusion in PKC-\u03b5-deficient mice than in WT mice one day after IRI. Acute tubular necrosis and neutrophil infiltration were markedly reduced in PKC-\u03b5-deficient mice. To determine whether this resistance to ischemia-reperfusion injury resulted from changes in local renal cells or infiltrating leukocytes, we studied a life-supporting renal transplant model of ischemic graft injury. We transplanted kidneys from H<jats:sup>2b<\/jats:sup> PKC-\u03b5-deficient mice (129\/SV) and their corresponding WT littermates into major histocompatibility complex-incompatible H<jats:sup>2d<\/jats:sup> recipients (BALB\/c) and induced ischemic graft injury by prolonged cold ischemia time. Recipients of WT allografts developed severe renal failure and died within 10 days of transplantation. Recipients of PKC-\u03b5-deficient allografts had better renal function and survival; they had less generation of ROS and upregulation of proinflammatory proteins (i.e., ICAM-1, inducible nitric oxide synthase, and TNF-\u03b1) and showed less tubular epithelial cell apoptosis and inflammation in their allografts. These data suggest that local renal PKC-\u03b5 expression mediates proapoptotic and proinflammatory signaling and that an inhibitor of PKC-\u03b5 signaling could be used to prevent hypoxia-induced AKI. <\/jats:p>","DOI":"10.1152\/ajprenal.00372.2013","type":"journal-article","created":{"date-parts":[[2014,7,24]],"date-time":"2014-07-24T02:48:09Z","timestamp":1406170089000},"page":"F718-F726","source":"Crossref","is-referenced-by-count":31,"title":["Renal PKC-\u03b5 deficiency attenuates acute kidney injury and ischemic allograft injury via TNF-\u03b1-dependent inhibition of apoptosis and inflammation"],"prefix":"10.1152","volume":"307","author":[{"given":"Song","family":"Rong","sequence":"first","affiliation":[{"name":"Department of Nephrology, Hannover Medical School, Hannover, Germany;"},{"name":"The Transplantation Center, Affiliated Hospital, Zunyi Medical College, Zunyi, 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