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CIDEC Is Involved in LPS-Induced Inflammation and Apoptosis in Renal Tubular Epithelial Cells

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Abstract

Adenosine 5′-monophosphate-activated protein kinase (AMPK) has been shown to have anti-inflammatory effect by inhibition of the nuclear factor κB (NF-κB) pathway and is involved in lipopolysaccharide (LPS)-induced inflammation. Cell-death-inducing DFF45-like effector C (CIDEC) can directly down-regulate AMPK activity through interacting with AMPKα subunit. However, whether the AMPK or CIDEC is involved in LPS-induced inflammation in renal tubular epithelial cells is still unknown. Therefore, we studied the role of AMPK and CIDEC in LPS-treated NRK-52E cells. Our results showed that LPS could up-regulate the expression of CIDEC in vitro and in vivo. Silencing CIDEC by CIDEC-siRNA could restore expression of phosphorylated-AMPKα which was decreased by LPS, suppress LPS-induced NF-κB pathway activation, and TNF-α, IL-6, and IL-1β production in NRK-52E cells. Furthermore, silencing CIDEC also partially alleviated LPS-induced epithelial cells apoptosis. In conclusion, the results demonstrated that CIDEC/AMPK signaling pathway played an important role in LPS-induced inflammation and epithelial cells apoptosis.

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Acknowledgments

We are grateful to Lixue Chen, Xiaojuan Deng, and jun He at the central laboratory of the First Affiliated Hospital of Chongqing Medical University for their assistance while we conducted our experiments.

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Contributions

J. He and B. Zhang conceived the study and designed the experiments. J. He, B. Zhang performed all of the experiments, analyzed the data, and wrote the manuscript. H. Gan reviewed and revised the paper.

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Correspondence to Hua Gan.

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The authors declare that they have no competing interest.

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He, J., Zhang, B. & Gan, H. CIDEC Is Involved in LPS-Induced Inflammation and Apoptosis in Renal Tubular Epithelial Cells. Inflammation 41, 1912–1921 (2018). https://doi.org/10.1007/s10753-018-0834-3

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