Tnfrsf11b
- Known as:
- Tnfrsf11b
- Catalog number:
- 043095A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Tnfrsf11b
Related genes to: Tnfrsf11b
- Gene:
- TNFRSF11B NIH gene
- Name:
- TNF receptor superfamily member 11b
- Previous symbol:
- OPG
- Synonyms:
- OCIF, TR1
- Chromosome:
- 8q24.12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2016-10-05
Related products to: Tnfrsf11b
Related articles to: Tnfrsf11b
- Postmenopausal osteoporosis (PMOP), characterized by excessive bone resorption and impaired bone remodeling, remains a significant global health challenge. This study investigated the protective effects of fucoidan from giant kelp (GKP) against PMOP and its underlying mechanisms in ovariectomized mice. GKP supplementation attenuated bone loss by preserving trabecular microarchitecture, normalizing systemic mineral homeostasis, and suppressing osteoclastogenesis, as evidenced by the downregulation of osteoclast-related genes. 16S rRNA gene sequencing revealed that GKP reshaped the gut microbiota by decreasing the Bacteroidota/Firmicutes ratio and enriching beneficial taxa, which promoted short-chain fatty acid production. Targeted metabolomics revealed that GKP induced profound systemic metabolic reprogramming, particularly amino acid metabolism, and identified betaine as a key systemic metabolite effector upregulated following GKP treatment. In vitro assays demonstrated that betaine suppressed receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation and mitigated inflammation. In vivo validation demonstrated that betaine intervention recapitulated the osteoprotective phenotype observed in GKP-treated mice, which was associated with regulation of the osteoprotegerin/RANKL/RANK signaling axis. These results indicate that GKP exerts anti-osteoporotic effects in association with changes in gut microbiota and systemic metabolism, while betaine-mediated regulation of the OPG/RANKL/RANK signaling may contribute to its osteoprotective activity. - Source: PubMed
Publication date: 2026/07/24
Ai ChunqingWang LuYe XingchenRen XiaomengSong ShuangLi Xuelu - Excessive fluoride intake can lead to skeletal fluorosis, which is a global public health concern. In recent years, selenium-loaded chitosan nanoparticles (CS-SeNPs) have attracted considerable attention due to their high bioactivity and favourable adhesion to the intestinal mucosa, and have demonstrated significant potential in mitigating skeletal damage. Nevertheless, it remains unclear whether CS-SeNPs can improve fluoride-induced bone damage and what the underlying regulatory mechanisms are. In this study, we found that CS-SeNPs alleviated fluoride-induced intestinal barrier disruption and colonic microbiota dysbiosis by downregulating pro-inflammatory and toxin-producing bacteria Desulfovibrio and Bilophila. CS-SeNPs increased the levels of beneficial bacteria such as Lactobacillus and Blautia, suppressed the expression of tumor necrosis factor (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6), and reduced reactive oxygen species (ROS) and malondialdehyde (MDA) levels, thereby improving systemic chronic inflammation and oxidative damage. Furthermore, CS-SeNPs also enhanced the absorption of calcium and phosphorus by bone tissue and, via the gut-bone axis, inhibited the sustained activation of the bone osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL)/nuclear factor kappa-B (NF-κB) pathway, as well as the abnormal activation of osteoclasts, thereby restoring bone metabolic balance and effectively alleviating fluoride-induced bone damage. These findings reveal the unique mechanisms of CS-SeNPs in regulating bone resorption and bone formation, not only providing new insights into the interaction between CS-SeNPs and the intestinal microbiota, but also offering potential therapeutic strategies for alleviating fluoride-induced bone damage. - Source: PubMed
Publication date: 2026/06/23
Zhao HuiZhao TianruiWang JiaxinLi YuanyuanLi HaojieShi TongzhouZhao YangfeiZhang JianhaiWang JundongCheng XiaofangWang Jinming - Osteoprotegerin (OPG), encoded by TNFRSF11B, plays a critical role in suppressing osteoclastogenesis as a secreted decoy receptor for RANKL. Loss-of-function mutations in TNFRSF11B cause juvenile Paget's disease and related bone metabolic disorders; however, the mechanisms by which individual mutations impair OPG secretion and function remain incompletely understood. Here, we quantitatively analyzed the effects of disease-associated TNFRSF11B variants on OPG secretion and osteoclastogenesis-inhibitory activity. Wild-type and variant OPG proteins were expressed as Gaussia luciferase fusion constructs to measure extracellular secretion, and functional activity was evaluated using a mouse osteoclastogenesis assay. The cysteine-substituted variants C65F and C87Y exhibited severe secretion defects, whereas the T76P and D182del variants showed reductions in both secretion and inhibitory activity. The F117L variant showed normal secretion but markedly reduced inhibitory activity, indicating a secretion-independent functional defect. In contrast, the truncation variants D323fs and R333Ter exhibited reduced secretion while retaining substantial anti-RANKL activity. Further analysis revealed that endoplasmic reticulum-associated degradation (ERAD) contributes to the regulation of OPG secretion. Proteasome inhibition and knockdown of the ERAD components HRD1 and SEL1L increased extracellular levels of wild-type OPG as well as those of D323fs and R333Ter variants. Collectively, our results define mutation-specific mechanisms underlying OPG dysfunction and identify ERAD as a regulator of OPG secretion. - Source: PubMed
Publication date: 2026/08/10
Suzuki ReinaNishida-Fukuda HisayoFukuda ShinjiShibata YutoSato TakumaMiyazawa KenSuzuki Takahiro - Intrinsic capacity (IC) reflects multidomain functional reserve and a measurable phenotype of healthy ageing, but its biological correlates remain incompletely understood. We examined associations of neurofilament light chain (NfL), CXCL9 and inflammatory biomarkers with IC in community-dwelling older adults. We conducted a cross-sectional analysis within the Screening and Prevention of Intrinsic Capacity Decline in Elders (SPICE) programme. IC was derived from locomotion (SPPB), cognition (MoCA), psychological health (PHQ-9), and vitality (MNA-SF), rescaled to a 0-100 composite and analysed as both z scores and tertiles. NfL, CXCL9, and TNFRSF11B were measured using Olink assays, and interleukin-6 (Il-6) by electrochemiluminescence. Multivariable linear and multinomial regression models assessed associations with IC. Mediation analyses evaluated indirect effects of inflammatory biomarkers via NfL. Among 199 participants (mean age 71.9 ± 5.2 years), NfL, CXCL9, IL-6, and TNFRSF11B increased across decreasing IC tertiles. In multivariate models, only NfL remained independently associated with IC (β - 0.41, 95% CI - 0.72 to - 0.12), with attenuation of other biomarkers after NfL adjustment. Higher NfL was associated with increased likelihood of low versus high IC (RRR 6.62, 95% CI 1.84-23.76). Mediation analyses showed significant indirect effects via NfL for CXCL9 (27.6%) and TNFRSF11B (53.9%), but not IL-6. Domain-specific analyses indicated distinct biomarker associations: NfL with locomotion and psychological health, IL-6 with locomotion, CXCL9 with vitality and TNFRSF11B with cognition. NfL was significantly associated with IC and partially mediated inflammatory associations. Integrating blood-based biomarkers with IC assessment may enhance early detection of multidomain vulnerability in ageing. - Source: PubMed
Publication date: 2026/08/04
Merchant Reshma AzizLiu YangTan Benjamin Y QSia Ching-HuiWong AndreaTan Li FengDuque GustavoArai HidenoriVellas BrunoWoo Jean - The cellular origin of smooth muscle cell (SMC)-derived populations in vascular lesions remains unresolved. Here we show, using single-cell transcriptomic analyses spanning carotid ligation injury, Myh11-CreERT-traced aortic homeostasis, and LDLR- and ApoE-deficient atherosclerosis, that a rare progenitor-like "Primed" SMC compartment pre-exists at baseline in all models and in the healthy human aorta. Relative to contractile SMCs, Primed SMCs attenuate sarcomeric and contractile programmes while inducing matricellular, progenitor-niche and chondrogenic-poised developmental programmes, resolving into conserved niche/progenitor () and matricellular () cores overlaid by vessel-specific signatures, on a retained SMC identity. Multiple orthogonal computational lineage-inference approaches indicate that this compartment expands predominantly through autonomous self-renewal and is the dominant inferred source of cycling and lesion fibrochondrocyte populations, while contractile SMCs are consistently depleted as a feeder source. These findings reframe lesional SMC cellularity as expansion of a pre-existing Primed compartment rather than widespread phenotypic switching of contractile SMCs. - Source: PubMed
Publication date: 2026/07/24
Wani ShwethaliKitching MichaelAboulhassanzadeh SobhanLungu Teodora-SimonaKilicgun IsilUlibarri KarsynLiu WeiminFloudas AchilleasRedmond Eileen MCahill Paul A