NDLI: TNF-alpha decreases ABCA1 expression and attenuates HDL cholesterol efflux in the human intestinal cell line Caco-2.

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TNF-alpha decreases ABCA1 expression and attenuates HDL cholesterol efflux in the human intestinal cell line Caco-2.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Field, F. Jeffrey Watt, Kim Mathur, Satya N.
Description	Author Affiliation: Field FJ ( Department of Internal, Medicine University of Iowa, Iowa City, IA 52242, USA. f-jeffrey-fi eld@uiowa.edu)
Abstract	HDL cholesterol levels are decreased in Crohn's disease, a tumor necrosis factor-alpha (TNF-alpha)-driven chronic inflammatory condition involving the gastrointestinal tract. ATP-binding cassette transporter A1 (ABCA1), one of several liver X receptor (LXR) target genes, is a cell surface transporter that mediates the rate-controlling step in HDL synthesis. The regulation of ABCA1 and HDL cholesterol efflux by TNF-alpha was investigated in the human intestinal cell line Caco-2. In response to cholesterol micelles or T0901317, an LXR nonsterol agonist, TNF-alpha decreased the basolateral efflux of cholesterol to apolipoprotein A1 (apoA1). TNF-alpha, by attenuating ABCA1 promoter activity, markedly decreased ABCA1 gene expression without attenuating the expression of LXR-alpha, LXR-beta, and most other LXR target genes, such as ABCG1, FAS, ABCG8, scavenger receptor-B1 (SR-B1), and apoC1. TNF-alpha also decreased ABCA1 mass by markedly enhancing the rate of ABCA1 degradation and modestly inhibiting its rate of synthesis. Inhibitors of the nuclear factor-kappaB (NF-kappaB) pathway, which is activated by TNF-alpha, partially reverse the effect of TNF-alpha on ABCA1 protein expression. The results suggest that TNF-alpha, the major cytokine implicated in the inflammation of Crohn's disease, decreases HDL cholesterol levels by attenuating the expression of intestinal ABCA1 and cholesterol efflux to apoA1.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M002410
Journal	The Journal of Lipid Research
Issue Number	6
Volume Number	51
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2010-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Atp-binding Cassette Transporters Genetics Cholesterol, Hdl Metabolism Gene Expression Regulation Drug Effects Intestines Cytology Tumor Necrosis Factor-alpha Pharmacology Atp Binding Cassette Transporter 1 Animals Caco-2 Cells Nf-kappa B Orphan Nuclear Receptors Signal Transduction Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

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Origins of intestinal ABCA1-mediated HDL-cholesterol

TNF-α decreases ABCA1 expression and attenuates HDL cholesterol efflux in the human intestinal cell line Caco-2

Molecular Mechanisms of Cellular Cholesterol $Efflux^{*}$

TNFalpha induces ABCA1 through NF-kappaB in macrophages and in phagocytes ingesting apoptotic cells.

Cholesterol efflux to apoA-I in ABCA1-expressing cells is regulated by $Ca^{2+}-dependent$ calcineurin signaling

Direct interaction of nuclear liver X receptor-beta with ABCA1 modulates cholesterol efflux.

The Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease

The macrophage cholesterol exporter ABCA1 functions as an anti-inflammatory receptor.

Binding of PDZ-RhoGEF to ATP-binding Cassette Transporter A1 (ABCA1) Induces Cholesterol Efflux through RhoA Activation and Prevention of Transporter Degradation

TNF-alpha decreases ABCA1 expression and attenuates HDL cholesterol efflux in the human intestinal cell line Caco-2.

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TNF-alpha decreases ABCA1 expression and attenuates HDL cholesterol efflux in the human intestinal cell line Caco-2.