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- W4315702928 abstract "Abstract Background Activation of the multifunctional Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) is a common intermediate of diverse stimuli-induced cell death. Suilysin(Sly) has toxicity on a variety of cells, however, the underlying mechanism of its effect remains unclear, and the mechanism of CaMKII in Sly-induced cell death has not been reported. Methods CaMKII expression in porcine kidney-15 (PK-15) was detected by RT-qPCR analysis and Western blotting. Morphological analysis, and CCK-8 assay were done to verify that CaMKII promotes cytotoxicity induced by Sly. AO/EB staining, and flow cytometry were used to probe into the role of CaMKII and reactive oxygen species (ROS) in Sly-induced apoptosis. The effect of CaMKII on Sly-induced toxicity in mice was evaluated by pathological tissue slices analysis. Results CaMKII was phosphorylated by Sly in PK-15, and inhibition or knockdown of CaMKII resulted in increased resistance to Sly. In PK-15 pretreated with a CaMKII inhibitor (KN93), Sly bound to the cell membrane was reduced, and the Sly-induced ROS, apoptosis were alleviated. Moreover, pretreatment with N-acetyl-L cysteine (NAC), a ROS scavenger, also blocked Sly-induced apoptosis. In summary, our study demonstrated that CaMKII activation and ROS production were involved in Sly-induced apoptosis. In addition, we identified that KN93 attenuated the damage of Sly to the viscera. Conclusion CaMKII participates in Sly-induced ROS-dependent apoptosis and the toxic effects of Sly in mice." @default.
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- W4315702928 date "2023-01-12" @default.
- W4315702928 modified "2023-09-30" @default.
- W4315702928 title "CaMKII promotes ROS-dependent apoptosis induced by Suilysin in PK-15 cells" @default.
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- W4315702928 doi "https://doi.org/10.21203/rs.3.rs-2450444/v1" @default.
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