在骨质细胞中抑制NFATc1表达的Curdlan诱导抑制的分子机制
Ayaka Koga1,2, Yoshie Nagai-Yoshioka2, Ryota Yamasaki2
1Department of Health Sciences, Kyushu Dental University, Kitakyushu, Fukuoka, Japan.
Journal of cellular biochemistry
|November 28, 2024
概括
库德兰是一种β-葡萄糖,通过抑制NFATc1.1.抑制骨质细胞形成,从而抑制骨质细胞形成. 这项研究揭示了curdlan通过dectin-1和补充受体3 (CR3) 途径来调节骨质细胞分化.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 骨质细胞对骨重塑和再吸收至关重要.
- 骨质细胞分化由涉及免疫受体的信号通路调节.
- 库德兰是一种β-葡萄糖,此前已被证明可以通过dectin-1抑制骨质细胞形成.
研究的目的:
- 阐明克尔德兰抑制RANKL诱导的骨质细胞分化的分子机制.
- 调查德-1和其他受体在克尔德兰抗骨质结晶效应中的作用.
主要方法:
- 实时RT-qPCR用于测量基因表达 (NFATc1).
- 西部斑点分析以评估蛋白质激活 (NF-κB通路).
- 耐酸盐性性酸酶染色用于骨质细胞分化.
- 使用中和抗体进行CR3阻断实验.
主要成果:
- 库德兰抑制了在过度表达dectin-1的细胞中的NFATc1表达.
- 库德兰在各种细胞系中抑制了RANKL诱导的NF-κB激活.
- 库德兰抑制了骨质细胞的分化,这表明了脱-1-独立的机制.
- 用抗体阻止CR3 (CD11b) 逆转了Curdlan抑制IκBα降解的作用.
结论:
- 库德兰通过依赖甲-1和依赖CR3的途径抑制骨质细胞分化.
- 库德兰通过CR3识别调节NF-κB通路来负面调节NFATc1表达.
- 研究结果提供了对代谢性骨病和炎症性骨损伤的潜在治疗策略的见解.
更多相关视频
07:51Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
Published on: March 18, 2019
5.9K
11:47A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
Published on: June 8, 2014
11.6K
相关概念视频
NF-κB-dependent Signaling Pathway
7.2K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
7.2K
Co-activators and Co-repressors
7.3K
Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
7.3K
Osteoclasts in Bone Remodeling
2.8K
Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
2.8K
TGF - β Signaling Pathway
7.2K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.2K
Receptor Downregulation in MVBs
2.0K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
2.0K
