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https://www.selleckchem.com/products/Camptothecine.html Recent advances on the role of the S1Pceramide rheostat in controlling the fate of villous trophoblasts and the role of S1P as a negative regulator of trophoblast syncytialization to a multinucleated placental barrier are discussed. This review also explores the role of S1P in anti-inflammatory and pro-inflammatory signaling, its role as a vasoconstrictor, and the effects of S1P metabolizing enzymes and receptors in pregnancy. Caspase-1 knockout mice (Casp1KO) are protected from Acute Kidney Injury (AKI) after warm ischemia/reperfusion injury in non-transplant models. Since Caspase-1 plays a central role as an inflammatory response initiator, we hypothesized that Casp1KO mice would be protected from AKI following transplant. Renal tubular cells (RTECs) were subjected to cold storage and rewarming (CS/REW). C57Bl/6J wild type or Casp1KO kidneys were subjected to CI for 30min and then transplanted into wild type recipients (CI+Txp). The recipients underwent bilateral native nephrectomy at the time of transplant. Serum creatinine (sCr) was measured 24h after native nephrectomy to assess transplant function. We found that RTECs subjected to CS/REW had significantly increased expression of the Caspase-1 and inflammasome protein NLRP1. Wild type kidneys subjected to CI+Txp into wild type recipients also demonstrated significantly increased Caspase-1 and NLRP1 protein expression compared to kidneys transplanted from Casp1KO donors into wild type recipients. Caspase-1 deletion results in significantly decreased RTEC apoptosis in transplanted Casp1KO vs WT kidneys. Surprisingly, however, renal function, ATN scores including brush border injury, cast formation and tubular simplification were similar in both groups and not significantly different. Our data suggest that other triggers of inflammation and programmed necrosis may need to be inhibited in addition to attenuating Caspase-1 to fully prevent AKI after kidney tran

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