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

Jin He1, Bin Zhang2, Hua Gan3,4

  • 1Department of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.

Inflammation
|July 1, 2018
PubMed

Insights

Cell-death-inducing DFF45-like effector C (CIDEC) promotes kidney inflammation by inhibiting Adenosine 5'-monophosphate-activated protein kinase (AMPK). Silencing CIDEC reduces inflammation and apoptosis in renal cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Adenosine 5'-monophosphate-activated protein kinase (AMPK) exhibits anti-inflammatory properties via Nuclear Factor-kappa B (NF-κB) pathway inhibition.
  • Lipopolysaccharide (LPS) induces inflammation, and Cell-death-inducing DFF45-like effector C (CIDEC) negatively regulates AMPK activity.

Purpose of the Study:

  • To investigate the roles of AMPK and CIDEC in LPS-induced inflammation in renal tubular epithelial cells (NRK-52E).
  • To elucidate the CIDEC/AMPK signaling pathway's involvement in renal inflammation and apoptosis.

Main Methods:

  • LPS treatment of NRK-52E cells in vitro and in vivo.
  • CIDEC silencing using CIDEC-siRNA.
  • Analysis of phosphorylated-AMPKα expression, NF-κB pathway activation, pro-inflammatory cytokine production (TNF-α, IL-6, IL-1β), and apoptosis.

Main Results:

  • LPS upregulated CIDEC expression in renal tubular epithelial cells.
  • CIDEC silencing restored LPS-impaired AMPK activity.
  • Silencing CIDEC suppressed LPS-induced NF-κB activation, pro-inflammatory cytokine release, and partially alleviated apoptosis.

Conclusions:

  • CIDEC plays a critical role in mediating LPS-induced inflammation and apoptosis in renal tubular epithelial cells.
  • The CIDEC/AMPK signaling pathway is a key regulator of renal inflammation and cell death in response to LPS.
Keywords:
AKIAMPKCIDECinflammation

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