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    • Previous studies have shown that remote IPC

    2018-10-23

    Previous studies have shown that remote IPC is involved in activation of multifactorial anti-inflammatory, neuronal, and humoral signaling pathways (Gassanov et al., 2014). For example, remote IPC could confer cardio-protection against ischemia through up-regulating erythropoietin (EPO) and hypoxia-inducible factor-1α (HIF1α) in the kidney (Oba et al., 2015). EPO preconditioning is also able to protect against cardiac and kidney I/R injury (Gardner et al., 2014). As such, some factors/molecules produced in the kidney may play a role in the defense mechanism of remote IPC. Thus, it will be interesting to identify novel kidney-secreted proteins contributing to renal protection under remote IPC. Among numerous candidates that exert a reno-protective effects, renalase is not only a kidney-originated amine oxidase, but also a molecule that is subjected to HIF-1 regulation at transcriptional level (Wang et al., 2015c, Du et al., 2015). It has been documented that renalase can regulate blood pressure and protect against both heart and kidney I/R injury (Lee et al., 2013; Wang et al., 2014a, 2014b, 2015a, 2015c; Du et al., 2015, Guo et al., 2014). Our previous study also demonstrated that exogenous administration of renalase was effective in alleviating CIN in rats (Zhao et al., 2015) and that local IPC induced buy 1-Deoxynojirimycin renalase upregulation via HIF-1α dependent mechanism. Furthermore, renalase plays a vital role in reno-protection of local IPC against I/R induced AKI (Wang et al., 2015c). In line with our observations, other studies showed that renalase expression was elevated and attenuated cardiac injury in mice challenged with cardiac I/R (Du et al., 2015). Recently, it has been reported that renalase may function as a pro-survival/growth factor and signals via the receptor plasma membrane calcium ATPase subtype 4b (PMCA4b) (Wang et al., 2015d, Guo et al., 2016). Nevertheless, there is no study to address the role of renalase in remote IPC against kidney I/R injury so far.
    Materials and methods
    Results
    Discussion Remote IPC, especially limb IPC, is a harmless, nonpharmacological and effective prevention and treatment strategy for I/R injury in many organs and has been widely used in clinical settings. Recent studies suggest that this approach is also effective for prevention of AKI (Wever et al., 2011) and CIN (Liu et al., 2015). In agreement with previous animal studies (Liu et al., 2015), we found that limb IPC attenuated deterioration of renal function after Ioversol-induced CIN, which was accompanied with reduced cell apoptosis, inflammation and oxidative stress. In addition, renalase, a kidney-derived protein was up-regulated after limb IPC whereas renalase knockdown eliminated the reno-protection of limb IPC as evidenced by our observations that rats pretreated with renalase siRNA exhibited more severe tubular injury and worsen renal function. These results are consistent with our previous study showing that exogenous renalase administration protected CIN through anti-oxidation, anti-inflammation and anti-apoptosis mechanisms (Zhao et al., 2015) and suggest that renalase plays a pivotal role in mediating the reno-protective effect of limb IPC. Mounting evidence has proved that renalase can mediates cytoprotection via activating survival-associated signaling such as Mitogen-activated protein kinase (MAPK) and Protein kinase B (AKT) (Wang et al., 2014b, 2015d). Recently, it has been reported that inhibition of renalase signaling has antitumor activity in pancreatic cancer and melanoma (Guo et al., 2016). Our previous study also demonstrated that local IPC-elicited beneficial effects on renal I/R injury was partly dependent renalase upregulation, which was associated with decreased apoptosis and oxidative stress. In this study, our findings confirmed that renalase plays an essential role in in remote IPC-elicited reno-protection against CIN, which contributes to a better understanding of the biological properties of renalase. Renalase, up-regulated under both local hypoxia and remote IPC, can promote cell survival and protect against I/R injury.