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TNF-α Downregulates CIDEC via MEK/ERK Pathway in Human Adipocytes

TNF-α Downregulates CIDEC via MEK/ERK Pathway in Human Adipocytes

Xinrui Tan, Zhenzhen Cao, Min Li, Erdi Xu, Jingjing Wang, Yanfeng Xiao

Obesity (Silver Spring). 2016 May;24(5):1070-80.

PMID: 27062372

Abstract:

Objective:
Cell death-inducing DFF45-like effector C (CIDEC) is a lipid droplet-coating protein that promotes triglyceride accumulation and inhibits lipolysis. TNF-α downregulates CIDEC levels to enhance basal lipolysis, whereas CIDEC overexpression could block this effect. This study aimed to investigate the signaling pathway of TNF-α-mediated CIDEC downregulation in human adipocytes.
Methods:
First CIDEC expression was detected in adipose tissue of lean and human subjects with obesity. Next, the temporal- and dose-dependent effects of TNF-α on CIDEC expression in human SW872 adipocytes were investigated. Selective inhibitors or RNAi or constitutively active MEK1 mutant was used to suppress or stimulate MEK/ERK cascade. Immunofluorescence and subcellular fractionation technique were used to study PPARγ redistribution after TNF-α treatment. Reporter assay was performed to confirm the direct effects of TNF-α on CIDEC transcription.
Results:
CIDEC expression decreased in adipose tissue of subjects with obesity and negatively correlated with adipose TNF-α levels and systemic lipolysis. TNF-α reduced CIDEC expression in vitro, but suppression of MEK/ERK cascade prevented TNF-α-mediated CIDEC downregulation. PPARγ, the transcription factor of CIDEC, was phosphorylated and redistributed by TNF-α in a MEK/ERK-dependent manner. Reporter assay confirmed that TNF-α reduced CIDEC transcription.
Conclusions:
TNF-α downregulates CIDEC expression through phosphorylation and nuclear export of PPARγ by MEK/ERK cascade.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4248889	TNF-α human			Price

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