LIGHT/TNFSF14 enhances adipose tissue inflammatory responses through its interaction with HVEM

Hong-Min Kim; Choon-Soo Jeong; Hye-Sun Choi; Teruo Kawada; Rina Yu

doi:10.1016/j.febslet.2011.01.011

LIGHT/TNFSF14 enhances adipose tissue inflammatory responses through its interaction with HVEM

FEBS Lett. 2011 Feb 4;585(3):579-84. doi: 10.1016/j.febslet.2011.01.011. Epub 2011 Jan 12.

Authors

Hong-Min Kim¹, Choon-Soo Jeong, Hye-Sun Choi, Teruo Kawada, Rina Yu

Affiliation

¹ Department of Biological Science, University of Ulsan, Nam-ku, Ulsan, South Korea.

PMID: 21236258
DOI: 10.1016/j.febslet.2011.01.011

Abstract

Obesity-induced adipose tissue inflammation is characterized by increased macrophage infiltration and cytokine production, and is associated with metabolic disorders. LIGHT/TNFSF14, a member of the TNF superfamily, plays a role in the development of various inflammatory diseases. The purpose of this study was to examine the involvement of soluble LIGHT (sLIGHT) in obesity-induced adipose tissue inflammatory responses. LIGHT gene expression on macrophages/adipocytes was upregulated by treatment with obesity-related factors. sLIGHT displayed chemotactic activity for macrophages and T cells, and enhanced inflammatory cytokine release from macrophages, adipocytes, and adipose tissue-derived SVF cells. The sLIGHT-induced inflammatory responses were blunted by neutralizing anti-HVEM antibody or knockout of HVEM, a receptor for sLIGHT. These findings indicate that sLIGHT enhances adipose tissue inflammatory responses through its interaction with HVEM.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adipocytes / metabolism
Adipose Tissue, White / cytology
Adipose Tissue, White / metabolism*
Animals
Cell Line
Cells, Cultured
Chemotaxis
Culture Media, Conditioned
Cytokines / metabolism*
Dietary Fats / administration & dosage
Gene Expression Regulation
Inflammation Mediators / metabolism*
Macrophages / metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Obesity / metabolism*
Oxidative Stress
RNA, Messenger / metabolism
Receptors, Tumor Necrosis Factor, Member 14 / antagonists & inhibitors
Receptors, Tumor Necrosis Factor, Member 14 / genetics
Receptors, Tumor Necrosis Factor, Member 14 / metabolism*
Stromal Cells / metabolism
Tumor Necrosis Factor Ligand Superfamily Member 14 / genetics
Tumor Necrosis Factor Ligand Superfamily Member 14 / metabolism*

Substances

Culture Media, Conditioned
Cytokines
Dietary Fats
Inflammation Mediators
RNA, Messenger
Receptors, Tumor Necrosis Factor, Member 14
Tnfrsf14 protein, mouse
Tnfsf14 protein, mouse
Tumor Necrosis Factor Ligand Superfamily Member 14