首页 > 最新文献

Journal of Oral Biosciences最新文献

英文 中文
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2026-01-01
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100750"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147018641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2026-01-01
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100736"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147018608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2026-01-01
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100740"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147018614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2026-01-01
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100742"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147018622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2026-01-01
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100719"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147018629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2026-01-01
{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100720"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147018630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Broad-range 16S rDNA sequencing and quantitative bacteriome profiling: a small-cohort feasibility study in orthodontic patients with early gingivitis 大范围16S rDNA测序和定量细菌组分析:早期牙龈炎正畸患者的小队列可行性研究
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2025-12-30 DOI: 10.1016/j.job.2025.100732
Tadaharu Yokogawa , Keiji Nagano , Hiroshi Miyakawa , Mari Fujita , Chen-Hsuan Chiu , Masahiro Iijima

Objectives

Many bacteriome studies employing next-generation sequencing (NGS) have focused on the partial sequencing of the 16S rRNA gene (rDNA). This limits both species-level resolution and quantitative interpretation of bacterial abundance, which have been addressed in this study.

Methods

Nanopore sequencing was used to analyze nearly the entire 16S rDNA sequence for species-level classification, and quantitative PCR for bacterial quantification. This approach was applied in a small-cohort feasibility study to investigate oral bacterial changes in orthodontic patients. Saliva samples were collected from 10 patients before and 1, 3, and 6 months after the initiation of orthodontic treatment.

Results

Dental caries was not detected during the study, and periodontal pockets ≥4 mm were rarely observed. However, all patients exhibited changes in bleeding on probing (BOP), which is indicative of early stage gingivitis. Although the compositional analysis did not reveal any significant association between specific bacterial species and BOP changes, the quantitative analysis showed a positive correlation between BOP changes and two bacterial species in the phyla Candidatus Saccharibacteria: Candidatus Saccharimonas aalborgensis and Candidatus Saccharibacteria bacterium oral taxon TM7x. No correlation was observed with representative periodontal disease-associated bacteria.

Conclusions

These findings support the feasibility of species-level and quantitative bacteriome analysis in a small cohort and highlight the bacterial species potentially linked to early stage gingivitis.
目的利用新一代测序技术(NGS)对细菌组的研究主要集中在16S rRNA基因(rDNA)的部分测序上。这限制了物种水平的分辨率和细菌丰度的定量解释,这在本研究中已经得到了解决。方法采用纳米孔测序法对几乎全部16S rDNA序列进行物种分类,采用定量PCR法对细菌进行定量分析。该方法应用于一项小队列可行性研究,以调查正畸患者口腔细菌的变化。收集10例患者在正畸治疗开始前、开始治疗后1、3、6个月的唾液样本。结果本研究未发现龋病,牙周袋≥4 mm者极少见。然而,所有患者都表现出探探出血(BOP)的变化,这是早期牙龈炎的指示。虽然成分分析未发现特定菌种与BOP变化之间存在显著相关性,但定量分析显示,BOP变化与Candidatus Saccharibacteria门中的两种细菌(Candidatus Saccharimonas aalborgensis和Candidatus Saccharibacteria口腔分类群TM7x)呈正相关。与代表性牙周病相关细菌无相关性。结论这些发现支持了在一个小队列中进行物种水平和定量细菌组分析的可行性,并突出了可能与早期牙龈炎相关的细菌种类。
{"title":"Broad-range 16S rDNA sequencing and quantitative bacteriome profiling: a small-cohort feasibility study in orthodontic patients with early gingivitis","authors":"Tadaharu Yokogawa ,&nbsp;Keiji Nagano ,&nbsp;Hiroshi Miyakawa ,&nbsp;Mari Fujita ,&nbsp;Chen-Hsuan Chiu ,&nbsp;Masahiro Iijima","doi":"10.1016/j.job.2025.100732","DOIUrl":"10.1016/j.job.2025.100732","url":null,"abstract":"<div><h3>Objectives</h3><div>Many bacteriome studies employing next-generation sequencing (NGS) have focused on the partial sequencing of the 16S rRNA gene (rDNA). This limits both species-level resolution and quantitative interpretation of bacterial abundance, which have been addressed in this study.</div></div><div><h3>Methods</h3><div>Nanopore sequencing was used to analyze nearly the entire 16S rDNA sequence for species-level classification, and quantitative PCR for bacterial quantification. This approach was applied in a small-cohort feasibility study to investigate oral bacterial changes in orthodontic patients. Saliva samples were collected from 10 patients before and 1, 3, and 6 months after the initiation of orthodontic treatment.</div></div><div><h3>Results</h3><div>Dental caries was not detected during the study, and periodontal pockets ≥4 mm were rarely observed. However, all patients exhibited changes in bleeding on probing (BOP), which is indicative of early stage gingivitis. Although the compositional analysis did not reveal any significant association between specific bacterial species and BOP changes, the quantitative analysis showed a positive correlation between BOP changes and two bacterial species in the phyla Candidatus <em>Saccharibacteria</em>: Candidatus <em>Saccharimonas aalborgensis</em> and Candidatus <em>Saccharibacteria</em> bacterium oral taxon TM7x. No correlation was observed with representative periodontal disease-associated bacteria.</div></div><div><h3>Conclusions</h3><div>These findings support the feasibility of species-level and quantitative bacteriome analysis in a small cohort and highlight the bacterial species potentially linked to early stage gingivitis.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100732"},"PeriodicalIF":2.3,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lineage tracing of Twist2-expressing cells in mouse taste buds 小鼠味蕾中twist2表达细胞的谱系追踪
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2025-12-30 DOI: 10.1016/j.job.2025.100729
Namiki Takaku-Tanoue , Kae Matsuyama , Takashi Toyono , Shinji Kataoka , Mitsushiro Nakatomi , Shingo Takai , Noriatsu Shigemura , Tatsuo Kawamoto , Yuji Seta

Objectives

It is widely accepted that Taste bud cells originate from the epithelium; however, evidence indicates that these cells are also derived from the mesenchyme beneath the epithelium. In this study, the cell lineage expressing Twist2, a transcription factor that is specifically expressed in the mesenchyme within taste buds, were examined to gain a deeper understanding of its biological characteristics.

Methods

Immunohistochemical analyses and taste organoid cultures were performed using Twist2 lineage-tracing reporter mice (Twist2-Cre mice crossed with tdTomato mice) to identify Twist2-derived cells in taste buds. The transgenic mice were harvested at 7, 14, and 21 days, post-administration of 5-ethynyl-2′-deoxyuridine (EdU), to assess the label retention of Twist2-derived cells.

Results

tdTomato-positive cells expressed Type III taste cell markers in the taste papillae and soft palate. tdTomato-positive organoids derived from the circumvallate papilla contained numerous taste bud cells. EdU analysis revealed that tdTomato-positive cells expressing a Type III taste cell marker persisted for longer than tdTomato-negative cells that expressed the same marker. In addition, almost all the long-term cultured tdTomato-positive organoids contained cells expressing a Type II taste cell marker.

Conclusions

The findings support the hypothesis that mesenchymal cells contribute to the taste bud cell population.
目的味蕾细胞起源于上皮细胞的观点已被广泛接受;然而,有证据表明这些细胞也来源于上皮下的间质。在这项研究中,我们研究了表达Twist2(一种在味蕾间质中特异性表达的转录因子)的细胞系,以更深入地了解其生物学特性。方法利用twist - cre小鼠(与tdTomato小鼠杂交)进行免疫组化分析和味觉类器官培养,鉴定味蕾中Twist2来源的细胞。在给予5-乙基-2 ' -脱氧尿苷(EdU)后的第7、14和21天收获转基因小鼠,以评估twist2来源细胞的标签保留情况。结果番茄阳性细胞在味觉乳头和软腭中表达III型味觉细胞标记物。番茄阳性的类器官来源于周围乳头,含有大量的味蕾细胞。EdU分析显示,表达III型味觉细胞标记的tdtomato阳性细胞比表达相同标记的tdtomato阴性细胞持续时间更长。此外,几乎所有长期培养的tdtomato阳性类器官都含有表达II型味觉细胞标记物的细胞。结论本研究结果支持了间充质细胞参与味蕾细胞群的假说。
{"title":"Lineage tracing of Twist2-expressing cells in mouse taste buds","authors":"Namiki Takaku-Tanoue ,&nbsp;Kae Matsuyama ,&nbsp;Takashi Toyono ,&nbsp;Shinji Kataoka ,&nbsp;Mitsushiro Nakatomi ,&nbsp;Shingo Takai ,&nbsp;Noriatsu Shigemura ,&nbsp;Tatsuo Kawamoto ,&nbsp;Yuji Seta","doi":"10.1016/j.job.2025.100729","DOIUrl":"10.1016/j.job.2025.100729","url":null,"abstract":"<div><h3>Objectives</h3><div>It is widely accepted that Taste bud cells originate from the epithelium; however, evidence indicates that these cells are also derived from the mesenchyme beneath the epithelium. In this study, the cell lineage expressing <em>Twist2</em>, a transcription factor that is specifically expressed in the mesenchyme within taste buds, were examined to gain a deeper understanding of its biological characteristics.</div></div><div><h3>Methods</h3><div>Immunohistochemical analyses and taste organoid cultures were performed using <em>Twist2</em> lineage-tracing reporter mice (<em>Twist2-Cre</em> mice crossed with <em>tdTomato</em> mice) to identify <em>Twist2</em>-derived cells in taste buds. The transgenic mice were harvested at 7, 14, and 21 days, post-administration of 5-ethynyl-2′-deoxyuridine (EdU), to assess the label retention of <em>Twist2</em>-derived cells.</div></div><div><h3>Results</h3><div>tdTomato-positive cells expressed Type III taste cell markers in the taste papillae and soft palate. tdTomato-positive organoids derived from the circumvallate papilla contained numerous taste bud cells. EdU analysis revealed that tdTomato-positive cells expressing a Type III taste cell marker persisted for longer than tdTomato-negative cells that expressed the same marker. In addition, almost all the long-term cultured tdTomato-positive organoids contained cells expressing a Type II taste cell marker.</div></div><div><h3>Conclusions</h3><div>The findings support the hypothesis that mesenchymal cells contribute to the taste bud cell population.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100729"},"PeriodicalIF":2.3,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Roles of the aryl hydrocarbon receptor and its ligands in osteoclast differentiation and temporomandibular joint osteoarthritis 芳烃受体及其配体在破骨细胞分化和颞下颌关节骨关节炎中的作用
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2025-12-23 DOI: 10.1016/j.job.2025.100726
Takashi Izawa , Islamy Rahma Hutami , Yuri Yoshikawa , Gohji Kozaki , Yusaku Hamada , Yuki Namba , Misa Taguchi , Jiamin Chen , Janvier Habumugisha , Hiroshi Kamioka

Background

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that plays an essential role in skeletal homeostasis. Increasing evidence indicates that AhR critically regulates osteoclast differentiation and activity, thereby influencing bone mass, bone resorption, and susceptibility to skeletal diseases. Although AhR has also been implicated in osteoblast-lineage cells, its regulatory roles in osteoclasts and immune cells are less well understood but are increasingly recognized as central to bone remodeling. In particular, AhR signaling modulates immune cell subsets relevant to bone metabolism and governs the differentiation of bone marrow-derived macrophages into osteoclasts.

Highlight

This review summarizes the recent findings regarding the regulation of osteoclast differentiation by AhR and its ligands under both physiological and pathological conditions. Special emphasis is placed on the interaction between AhR and the RANKL signaling axis in osteoclasts, as well as on how exogenous and endogenous ligands, including benzo[a]pyrene (B[a]P) and 6-formylindolo[3,2-b]carbazole (FICZ), modulate bone resorption and subchondral bone remodeling in temporomandibular joint osteoarthritis. Furthermore, the role of macrophages as osteoclast progenitors and immunomodulators has been highlighted, positioning AhR as a critical intermediary that links environmental exposure, inflammation, and skeletal metabolism.

Conclusion

In this review, we outlined the diverse functions of AhR signaling and its ligands in oral and temporomandibular joint osteoarthritis. AhR plays a central role in bone remodeling. The harmful exogenous ligand B[a]P generally promotes bone loss, whereas the endogenous ligand FICZ exerts protective actions. These insights highlight AhR as a key regulatory switch linking the skeletal and immune systems and as a promising therapeutic target for bone-destructive disorders.
芳烃受体(AhR)是一种配体激活的转录因子,在骨骼稳态中起重要作用。越来越多的证据表明,AhR对破骨细胞的分化和活性起关键调节作用,从而影响骨量、骨吸收和对骨骼疾病的易感性。虽然AhR也与成骨细胞谱系有关,但其在破骨细胞和免疫细胞中的调节作用尚不清楚,但越来越多的人认识到AhR是骨重塑的核心。特别是,AhR信号调节与骨代谢相关的免疫细胞亚群,并控制骨髓源性巨噬细胞向破骨细胞的分化。本文综述了近年来有关AhR及其配体在生理和病理条件下调控破骨细胞分化的研究进展。特别强调AhR与破骨细胞中RANKL信号轴之间的相互作用,以及外源性和内源性配体,包括苯并[a]芘(B[a]P)和6-甲酰基林多洛[3,2- B]咔唑(FICZ),如何调节颞下颌关节骨性关节炎的骨吸收和软骨下骨重塑。此外,巨噬细胞作为破骨细胞祖细胞和免疫调节剂的作用已被强调,将AhR定位为连接环境暴露、炎症和骨骼代谢的关键中介。结论本文综述了AhR信号及其配体在口腔和颞下颌关节骨性关节炎中的多种功能。AhR在骨重塑中起核心作用。有害的外源性配体B[a]P通常促进骨质流失,而内源性配体FICZ则发挥保护作用。这些见解强调了AhR作为连接骨骼和免疫系统的关键调节开关,以及作为骨破坏性疾病的有希望的治疗靶点。
{"title":"Roles of the aryl hydrocarbon receptor and its ligands in osteoclast differentiation and temporomandibular joint osteoarthritis","authors":"Takashi Izawa ,&nbsp;Islamy Rahma Hutami ,&nbsp;Yuri Yoshikawa ,&nbsp;Gohji Kozaki ,&nbsp;Yusaku Hamada ,&nbsp;Yuki Namba ,&nbsp;Misa Taguchi ,&nbsp;Jiamin Chen ,&nbsp;Janvier Habumugisha ,&nbsp;Hiroshi Kamioka","doi":"10.1016/j.job.2025.100726","DOIUrl":"10.1016/j.job.2025.100726","url":null,"abstract":"<div><h3>Background</h3><div>The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that plays an essential role in skeletal homeostasis. Increasing evidence indicates that AhR critically regulates osteoclast differentiation and activity, thereby influencing bone mass, bone resorption, and susceptibility to skeletal diseases. Although AhR has also been implicated in osteoblast-lineage cells, its regulatory roles in osteoclasts and immune cells are less well understood but are increasingly recognized as central to bone remodeling. In particular, AhR signaling modulates immune cell subsets relevant to bone metabolism and governs the differentiation of bone marrow-derived macrophages into osteoclasts.</div></div><div><h3>Highlight</h3><div>This review summarizes the recent findings regarding the regulation of osteoclast differentiation by AhR and its ligands under both physiological and pathological conditions. Special emphasis is placed on the interaction between AhR and the RANKL signaling axis in osteoclasts, as well as on how exogenous and endogenous ligands, including benzo[<em>a</em>]pyrene (B[<em>a</em>]P) and 6-formylindolo[3,2-<em>b</em>]carbazole (FICZ), modulate bone resorption and subchondral bone remodeling in temporomandibular joint osteoarthritis. Furthermore, the role of macrophages as osteoclast progenitors and immunomodulators has been highlighted, positioning AhR as a critical intermediary that links environmental exposure, inflammation, and skeletal metabolism.</div></div><div><h3>Conclusion</h3><div>In this review, we outlined the diverse functions of AhR signaling and its ligands in oral and temporomandibular joint osteoarthritis. AhR plays a central role in bone remodeling. The harmful exogenous ligand B[<em>a</em>]P generally promotes bone loss, whereas the endogenous ligand FICZ exerts protective actions. These insights highlight AhR as a key regulatory switch linking the skeletal and immune systems and as a promising therapeutic target for bone-destructive disorders.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100726"},"PeriodicalIF":2.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145839801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RANKL enhances the expression of PEPT1/SLC15A1 and PEPT2/SLC15A2 in RAW264.7 cells RANKL可增强RAW264.7细胞中PEPT1/SLC15A1和PEPT2/SLC15A2的表达
IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Pub Date : 2025-12-20 DOI: 10.1016/j.job.2025.100724
Mana Shintani , Wakana Sugimoto , Hiroshi Inoue , Nagako Sougawa , Seiji Goda , Aki Nishiura

Objectives

Muramyl dipeptide (MDP), a bacterial cell wall component, is recognized by NOD2 and vital in innate immune responses, including inflammatory cytokine production. MDP is transported into the cells via PEPT1/SLC15A1 and PEPT2/SLC15A2, which are members of the proton-coupled oligopeptide transporter family within the SLC15 solute carrier group. Although the effects of RANKL stimulation on certain transporters are known, its effects on the SLC15 family remain unclear. This study aimed to clarify the effects of RANKL stimulation on PEPT1/SLC15A1 and PEPT2/SLC15A2 in RAW264.7 cells and determine their role in osteoclast differentiation.

Methods

RAW264.7 cells were stimulated with RANKL and MDP. Expression levels of NOD2, PEPT1/SLC15A1, PEPT2/SLC15A2, cathepsin K, and NFATc1 were analyzed via Western blotting. Osteoclast differentiation was evaluated using a tartrate-resistant acid phosphatase (TRAP) activity assay.

Results

RANKL stimulation increased NOD2, PEPT1/SLC15A1, and PEPT2/SLC15A2 expression in RAW264.7 cells. Colistin and polymyxin B, which are PEPT1 and PEPT2 inhibitors, respectively, did not affect the stimulation of cells with RANKL alone. However, RANKL and MDP co-stimulation suppressed the RANKL/MDP-induced increase in TRAP activity and cathepsin K and NFATc1 expression.

Conclusions

RANKL stimulation increased PEPT1/SLC15A1 and PEPT2/SLC15A2 levels in RAW264.7 cells, suggesting an increase in the intracellular uptake of MDP. This may promote osteoclast differentiation, potentially through NOD2activation or NOD2-independent mechanisms.
目的:muramyl二肽(MDP)是一种细菌细胞壁成分,被NOD2识别,在先天性免疫反应中至关重要,包括炎症细胞因子的产生。MDP通过PEPT1/SLC15A1和PEPT2/SLC15A2转运到细胞中,它们是SLC15溶质载体群中质子偶联寡肽转运蛋白家族的成员。虽然RANKL刺激对某些转运蛋白的影响是已知的,但其对SLC15家族的影响尚不清楚。本研究旨在阐明RANKL刺激对RAW264.7细胞PEPT1/SLC15A1和PEPT2/SLC15A2的影响,并确定其在破骨细胞分化中的作用。Western blotting分析NOD2、PEPT1/SLC15A1、PEPT2/SLC15A2、cathepsin K、NFATc1的表达水平。使用抗酒石酸酸性磷酸酶(TRAP)活性测定来评估破骨细胞分化。结果rankl刺激可增加RAW264.7细胞中NOD2、PEPT1/SLC15A1和PEPT2/SLC15A2的表达。粘菌素和多粘菌素B分别是PEPT1和PEPT2抑制剂,单独使用RANKL对细胞的刺激没有影响。然而,RANKL和MDP共同刺激抑制了RANKL/MDP诱导的TRAP活性和组织蛋白酶K和NFATc1表达的增加。结论rankl刺激增加了RAW264.7细胞中PEPT1/SLC15A1和PEPT2/SLC15A2的水平,表明MDP的细胞内摄取增加。这可能通过nod2激活或nod2独立机制促进破骨细胞分化。
{"title":"RANKL enhances the expression of PEPT1/SLC15A1 and PEPT2/SLC15A2 in RAW264.7 cells","authors":"Mana Shintani ,&nbsp;Wakana Sugimoto ,&nbsp;Hiroshi Inoue ,&nbsp;Nagako Sougawa ,&nbsp;Seiji Goda ,&nbsp;Aki Nishiura","doi":"10.1016/j.job.2025.100724","DOIUrl":"10.1016/j.job.2025.100724","url":null,"abstract":"<div><h3>Objectives</h3><div>Muramyl dipeptide (MDP), a bacterial cell wall component, is recognized by NOD2 and vital in innate immune responses, including inflammatory cytokine production. MDP is transported into the cells via PEPT1/SLC15A1 and PEPT2/SLC15A2, which are members of the proton-coupled oligopeptide transporter family within the SLC15 solute carrier group. Although the effects of RANKL stimulation on certain transporters are known, its effects on the SLC15 family remain unclear. This study aimed to clarify the effects of RANKL stimulation on PEPT1/SLC15A1 and PEPT2/SLC15A2 in RAW264.7 cells and determine their role in osteoclast differentiation.</div></div><div><h3>Methods</h3><div>RAW264.7 cells were stimulated with RANKL and MDP. Expression levels of NOD2, PEPT1/SLC15A1, PEPT2/SLC15A2, cathepsin K, and NFATc1 were analyzed via Western blotting. Osteoclast differentiation was evaluated using a tartrate-resistant acid phosphatase (TRAP) activity assay.</div></div><div><h3>Results</h3><div>RANKL stimulation increased NOD2, PEPT1/SLC15A1, and PEPT2/SLC15A2 expression in RAW264.7 cells. Colistin and polymyxin B, which are PEPT1 and PEPT2 inhibitors, respectively, did not affect the stimulation of cells with RANKL alone. However, RANKL and MDP co-stimulation suppressed the RANKL/MDP-induced increase in TRAP activity and cathepsin K and NFATc1 expression.</div></div><div><h3>Conclusions</h3><div>RANKL stimulation increased PEPT1/SLC15A1 and PEPT2/SLC15A2 levels in RAW264.7 cells, suggesting an increase in the intracellular uptake of MDP. This may promote osteoclast differentiation, potentially through NOD2activation or NOD2-independent mechanisms.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100724"},"PeriodicalIF":2.3,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Journal of Oral Biosciences
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1