Ask about this productRelated genes to: TM7SF4 antibody
- Gene:
- DCSTAMP NIH gene
- Name:
- dendrocyte expressed seven transmembrane protein
- Previous symbol:
- TM7SF4
- Synonyms:
- DC-STAMP, FIND
- Chromosome:
- 8q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-25
- Date modifiied:
- 2014-11-19
Related products to: TM7SF4 antibody
Related articles to: TM7SF4 antibody
- Titanium implants are widely used in orthopedic and dental fields but often face challenges such as insufficient osseointegration and peri-implant inflammation. While Strontium (Sr) possesses potent bioactive properties, achieving its controlled delivery at the implant-tissue interface remains technically challenging. To address this, we engineered a multidimensional composite coating by constructing a micro/nano-porous TiO substrate via micro-arc oxidation (MAO), followed by polydopamine (PDA)-assisted Sr immobilization. This integrated architecture significantly enhanced surface hydrophilicity and facilitated high-content Sr loading with sustained release kinetics. Biological evaluations demonstrated that the PDA-mediated interface promoted superior initial adhesion and spreading of bone marrow mesenchymal stem cells (BMSCs), synergizing with released Sr to markedly upregulate core osteogenic markers (, ). Crucially, the functionalized surface actively optimized the immune microenvironment by inducing M1-to-M2 macrophage polarization and comprehensively suppressing RANKL-induced osteoclastogenesis via the downregulation of TRAP and DC-STAMP. By integrating these pro-osteogenic, anti-inflammatory, and anti-resorptive capabilities, this tri-functional system effectively rebalances the bone remodeling microenvironment. Consequently, it provides a robust, universally applicable strategy for enhancing the therapeutic efficacy of next-generation orthopedic and dental implants. - Source: PubMed
Publication date: 2026/04/07
Yang YimingLiu RongpuZhou YuqiYuan LingjunLi ZhenxiaLiao QianFang Bing - The effects of vanadyl acetylacetonate (VAC) were evaluated on femur intramedullary osteoclasts in a rat model of type 1 diabetes (T1D) associated bone remodeling. In this study, BB Wistar rats were administered intramedullary injections consisting of either VAC at a dose of 1.5 mg/kg or a control saline solution. These injections were administered at least 12 weeks after the onset of T1D (i.e., treatment began ≥ 12 weeks after diabetes onset) to allow for the establishment of diabetic bone changes. At 4 weeks following treatment, the femurs treated with VAC exhibited a significant increase in trabecular thickness, specifically a 19.03% increase (p < 0.05). Osteoclasts, which were identified using TRAP staining, were found to be reduced in number at both 6 and 8 weeks in the femurs that received VAC treatment (p < 0.05). Likewise, when VAC was added to culture media, it resulted in a substantial decrease in osteoclast formation in vitro (8.1 ± 16.8 vs. 91.6 ± 16.0 cells, p < 0.001). In addition, expression of Dcstamp was significantly decreased in VAC-treated femurs compared to those treated with saline (p < 0.05). Taken together, this study demonstrates that intramedullary VAC delivery appears to inhibit T1D-related bone loss by impairing the process of osteoclastogenesis. - Source: PubMed
Publication date: 2026/04/03
Greendyk JoshuaThornton JamesNapoleon DarianGreenberg MichaelLin AnthonyLevidy MikeLopez Jonathan RMuñoz MaximilianInnella KevinKadkoy YazanCulbertson Maya DezaCottrell Jessica AO'Connor J PatrickBenevenia JosephPaglia David NLin Sheldon S - Hydrogen sulfide (HS) is a novel gasotransmitter produced in mammalian cells and is known to various regulate physiological functions. Previous study reported that an imbalance in HS metabolism is associated with defective bone homeostasis. However, the detailed mechanism of how HS affect osteoclast differentiation remains unclear. In the present study, we demonstrated that the effect of HS donor GYY4137 on osteoclast differentiation and multi-nucleation. Treatment of GYY4137 significantly decreased the number of receptor activator of nuclear factor kappa-B ligand (RANKL)-induced tartrate-resistant acid phosphatase (TRAP)-positive cells and inhibited the expression of osteoclast-related genes, nuclear factor of activated T-cells 1 (NFATc1) and Cathepsin K(Ctsk). Additionally, the increased gene expression of dendritic cell-specific transmembrane protein (DC-STAMP), osteoclast stimulatory transmembrane protein (OC-STAMP), and v-ATPase V0 subunit d2 (Atp6v0d2), which are cell-cell fusion-related molecules by RANKL treatment, was attenuated by GYY4137. Furthermore, GYY4137 suppressed the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, JNK1/2, and p38MAPK, compared to RANKL-treated cells. Thus, our data suggested that HS donor GYY4137 as a novel osteoclast genesis inhibitor, significantly decreases osteoclast differentiation and multi-nucleation by inhibiting the expression of the cell-cell fusion molecules. - Source: PubMed
Takagi TomohiroInoue HirofumiMorimoto HiromuTakahashi NobuyukiUehara Mariko - Excessive osteoclast fusion and activation are central drivers of bone erosion in inflammatory osteopathies, which are closely linked to immune dysregulation. Wilforine, a natural compound, exhibits immunomodulatory and therapeutic potential, yet its precise mechanism of action-particularly its influence on the osteoclast membrane microenvironment and associated immune signaling-remains incompletely understood. - Source: PubMed
Publication date: 2026/03/13
Geng ShaohuiGuan YiweiYe ZiZhao DongdongJiang YijinFu JingyuanSheng HanYang ShuhanLiu HongxuDeng FuwenYu ShashaYimingjiang MureziyaWu YuanhaoLi ChenHuang Guangrui - : Bone remodeling depends on the dynamic balance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Follistatin-like 1 (FSTL1) has been reported as an osteoclast-secreted protein that inhibits osteoclast differentiation, but its direct effects on osteoblast differentiation remain unclear. This study aimed to determine whether FSTL1 regulates osteoblast differentiation and mesenchymal stem cell migration and characterizes its role in osteoclast-osteoblast cellular cross-talk under conditions. : Bone marrow-derived macrophages (BMMs) and stromal cells (BMSCs) from mice were used to induce osteoclast and osteoblast differentiation, respectively. Chemotaxis was assessed by Transwell migration, and osteoblast differentiation was evaluated in BMSC and MC3T3-E1 cells using staining, qRT-PCR, Western blotting, and proliferation assays. : FSTL1 significantly suppressed osteoclast differentiation and resorptive activity, confirmed by TRAP staining and pit assay, respectively. Expression of osteoclast markers such as NFATc1, TRAP, and DC-STAMP was reduced under FSTL1 treatment. In BMSCs, FSTL1 did not affect proliferation but significantly enhanced chemotaxis. Moreover, FSTL1 promoted osteogenic differentiation and mineralization, as demonstrated by increased ALP activity and Alizarin Red S staining. In MC3T3-E1 pre-osteoblasts, FSTL1 increased cell proliferation and mineralization by MTS and Alizarin Red staining. Key osteogenic markers, including Runx2 and osteocalcin, were also upregulated. : Osteoclast-derived FSTL1 significantly suppresses osteoclastogenesis and promotes mesenchymal cell chemotaxis and osteogenic differentiation, indicating a role in regulating osteoclast-osteoblast cellular interactions . Targeting FSTL1 signaling may represent a promising therapeutic strategy for osteoporosis and other disorders of impaired bone remodeling. - Source: PubMed
Publication date: 2026/02/28
Piao YongxuChe XiangguoJin XianLee Dong-KyoPark MinHeo Eun-JungOh JinyoungKim Seong-GonCho Dae-ChulKim Hyun-JuChoi Je-Yong