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TNFRSF14 deficiency protects against ovariectomy-induced adipose tissue inflammation
Eun-Kyung Choi1, Woon-Ki Kim, Ok-Joo Sul
1Department 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.
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.
Insights
Tumor necrosis factor receptor superfamily member 14 (TNFRSF14) drives adipose tissue inflammation and metabolic issues after ovarian function loss. TNFRSF14 deficiency protected against these post-ovariectomy effects, suggesting it as a therapeutic target.
Area of Science:
- Immunology
- Metabolism
- Endocrinology
Background:
- Loss of ovarian function, such as through ovariectomy (OVX), is linked to metabolic disturbances and adipose tissue (AT) inflammation.
- Tumor necrosis factor receptor superfamily member 14 (TNFRSF14) plays a role in immune responses and inflammation.
Purpose of the Study:
- To investigate the role of TNFRSF14 in metabolic dysfunction and AT inflammation following OVX.
- To determine if TNFRSF14 deficiency offers protection against OVX-induced metabolic perturbations.
Main Methods:
- Ovariectomy was performed in wild-type and TNFRSF14-knockout mice.
- Flow cytometry was used to analyze immune cell infiltration in adipose tissue.
- Glucose metabolism was assessed in the experimental models.
Main Results:
- OVX increased fat mass and CD11c+ inflammatory cell infiltration in AT, leading to impaired glucose metabolism.
- TNFRSF14 deficiency attenuated OVX-induced increases in fat mass and CD11c+ cell recruitment to AT.
- TNFRSF14 deficiency reduced M1 macrophage polarization and protected against glucose metabolism disturbance.
- TNFRSF14 engagement by its ligand LIGHT enhanced CD11c expression via reactive oxygen species generation.
Conclusions:
- TNFRSF14 mediates OVX-induced adipose tissue inflammation and metabolic dysfunction through CD11c upregulation.
- TNFRSF14 acts as a redox modulator, contributing to inflammation.
- TNFRSF14 represents a potential therapeutic target for managing postmenopausal syndrome by mitigating adipose tissue inflammation.
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