title: TNFRSF14 deficiency protects against ovariectomy-induced adipose tissue inflammation.
abstract: To elucidate the role of tumor necrosis factor receptor superfamily member 14 (TNFRSF14) in metabolic disturbance due to loss of ovarian function, ovariectomy (OVX) was performed in TNFRSF 14-knockout mice. OVX increased fat mass and infiltration of highly inflammatory CD11c cells in the adipose tissue (AT), which was analyzed by flow cytometry, and resulted in disturbance of glucose metabolism, whereas TNFRSF14 deficiency attenuated these effects. TNFRSF14 deficiency decreased recruitment of CD11c-expressing cells in AT and reduced the polarization of bone marrow-derived macrophages to M1. Upon engagement of LIGHT, a TNFRSF14 ligand, TNFRSF14 enhanced the expression of CD11c via generation of reactive oxygen species, suggesting a role of TNFRSF14 as a redox modulator. TNFRSF14 participated in OVX-induced AT inflammation via upregulation of CD11c, resulting in metabolic perturbation. TNFRSF14 could be used as a therapeutic target for the treatment of postmenopausal syndrome by reducing AT inflammation.
authors.affiliation: Department of Biological Sciences, University of Ulsan, Ulsan 680-749, Korea Department of Endocrinology, Ulsan University Hospital, Ulsan 682-714, Korea Department of Pathology, Ulsan University Hospital, Ulsan 682-714, Korea Department of Food Science and Nutrition, University of Ulsan, Ulsan 680-749, Korea.
authors.forename: Eun-Kyung
authors.initials: EK
authors.lastname: Choi
authors.forename: Woon-Ki
authors.initials: WK
authors.lastname: Kim
authors.forename: Ok-Joo
authors.initials: OJ
authors.lastname: Sul
authors.forename: Yun-Kyung
authors.initials: YK
authors.lastname: Park
authors.forename: Eun-Sook
authors.initials: ES
authors.lastname: Kim
authors.forename: Jae-Hee
authors.initials: JH
authors.lastname: Suh
authors.forename: Rina
authors.initials: R
authors.lastname: Yu
authors.forename: Hye-Seon
authors.initials: HS
authors.lastname: Choi
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D039521:CD11c Antigen / Q000235:genetics / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D002478:Cells, Cultured; D004734:Energy Metabolism / Q000235:genetics; D005260:Female; D005434:Flow Cytometry; D015870:Gene Expression; D007249:Inflammation / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D018655:Lymphocyte Count; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010052:Ovariectomy; D017382:Reactive Oxygen Species / Q000378:metabolism; D053240:Receptors, Tumor Necrosis Factor, Member 14 / Q000172:deficiency* / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000378:metabolism
chemical_list: D039521:CD11c Antigen; D017382:Reactive Oxygen Species; D053240:Receptors, Tumor Necrosis Factor, Member 14; C506029:Tnfrsf14 protein, mouse; C505915:Tnfsf14 protein, mouse; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14
keywords: adipose tissue; glucose metabolism; inflammatory diseases; menopause; ovarian function