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

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.