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Ingenuity pathway analysis of gingival epithelial cells stimulated with estradiol and progesterone 雌二醇和孕酮刺激牙龈上皮细胞的摄取途径分析。
IF 2.4 Q2 Dentistry Pub Date : 2024-03-01 DOI: 10.1016/j.job.2023.11.002
Nodoka Sugiyama , Osamu Uehara , Yutaka Kawano , Durga Paudel , Tetsuro Morikawa , Norihiro Nakamoto , Satsuki Kato , Tetsuji Takayama , Toshiyuki Nagasawa , Hiroko Miura , Yoshihiro Abiko , Yasushi Furuichi

Objective

Periodontal disease is a risk factor for preterm delivery, and elevated female hormone levels during pregnancy promote hormone-dependent periodontopathogenic bacterial growth and gingivitis. Although the saliva of pregnant women contains female hormones at elevated levels, their effects on the gingiva are poorly understood. Therefore, in this study, we investigated the effects of estradiol and progesterone stimulation on gingival epithelial cells via ingenuity pathway analysis.

Methods

Human gingival epithelial progenitors were cultured in a CnT-Prime medium; 17β-estradiol (E2) and progesterone (P4) were used as the reagents. Cells treated with dimethyl sulfoxide alone were used as the control group. Cells in the control and experimental groups were incubated for 12 h. RNA was extracted from the cultured cells, RNA-Seq was performed, and pathway analysis was conducted.

Results

Differentially expressed genes were detected for 699 (over 2-fold increase) and 348 (decrease) genes in group E2 and for 1448 (increase) and 924 (decrease) genes in group P4 compared with those in the control group (FDR <0.05, n = 4). The z-scores of the pathways suggest that E2 and P4 increased the activity of the wound healing signaling pathway. The activation of this pathway was higher in the E2 and P4 groups than that in the control group.

Conclusions

The results of this study suggest that estradiol and progesterone may affect gingival homeostasis and wound healing.

目的:牙周病是早产的危险因素,妊娠期女性激素水平升高会促进激素依赖性牙周病致病菌生长和牙龈炎。尽管孕妇的唾液中含有较高水平的雌性激素,但人们对其对牙龈的影响知之甚少。因此,在本研究中,我们通过独创性通路分析研究了雌二醇和孕酮刺激对牙龈上皮细胞的影响。方法:在CnT Prime培养基中培养人牙龈上皮祖细胞;17β-雌二醇(E2)和孕酮(P4)作为试剂。使用单独用二甲基亚砜处理的细胞作为对照组。对照组和实验组中的细胞孵育12 h.从培养的细胞中提取RNA,进行RNA-Seq,并进行通路分析。结果:与对照组相比,E2组的699个(增加2倍以上)和348个(减少)基因以及P4组的1448个(增加)和924个(降低)基因存在差异表达(FDR结论:本研究结果表明雌二醇和孕酮可能影响牙龈稳态和伤口愈合。
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引用次数: 0
Disruption of CADM1-dependent cell-cell adhesion in human oral squamous cell carcinoma cells results in tumor progression, possibly through an increase of MMP-2 and MMP-9 expression 人口腔鳞状细胞癌细胞中cadm1依赖性细胞-细胞粘附的破坏导致肿瘤进展,可能是通过增加MMP-2和MMP-9的表达。
IF 2.4 Q2 Dentistry Pub Date : 2024-03-01 DOI: 10.1016/j.job.2023.11.005
Nanami Obara , Seiko Kyakumoto , Satoshi Yamaguchi , Hiroyuki Yamada , Akira Ishisaki , Masaharu Kamo

Objectives

This study aimed to clarify the molecular mechanism underlying the higher invasion and metastasis abilities of LMF4 cells than those of HSC-3 cells by comparing the expression levels of the tumor suppressor factor, cell adhesion molecule 1 (CADM1).

Methods

We explored 1) whether CADM1 expression level was downregulated in LMF4 cells compared with HSC-3 cells, 2) whether CADM1 expression knockdown increased the expression levels of matrix metalloproteinases (MMPs), 3) the exact cellular signaling pathways responsible for increased MMP expression after knockdown of CADM1 expression, and 4) whether disruption of CADM1-dependent HSC-3 cell adhesion increased the migratory and invasive activities of HSC-3 cells.

Results

CADM1 expression was lower in the LMF4 than in the HSC-3 cells. The knockdown of CADM1 increased the expression of MMP-2 and MMP-9 in HSC-3 cells. In addition, the upregulation of MMP-2 expression after CADM1 knockdown was abrogated by the mitogen-activated protein (MAP)/extracellular signal-regulated kinase kinase (MEK) inhibitor U0126 and the phosphoinositide 3-kinase (PI3K) inhibitor LY294002. The upregulation of MMP-9 expression after the knockdown of CADM1 was abrogated by the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the p38 MAP kinase (MAPK) inhibitor SB203580 and LY294002. Anti-CADM1 neutralizing antibody evoked migratory and invasive abilities of HSC-3 cells.

Conclusion

The disruption of CADM1-dependent cell-cell adhesion in human oral squamous cell carcinoma cells resulted in tumor progression, possibly through an increase in MMP-2 expression in a MEK/PI3K-dependent manner and an increase in MMP-9 expression in a JNK/p38 MAPK/PI3K-dependent manner.

目的:本研究旨在通过比较肿瘤抑制因子细胞粘附分子1 (CADM1)的表达水平,阐明LMF4细胞高于HSC-3 细胞侵袭转移能力的分子机制。方法:研究1)与HSC-3 细胞相比,LMF4细胞中CADM1的表达水平是否下调;2)CADM1表达下调是否增加基质金属蛋白酶(MMPs)的表达水平;3)CADM1表达下调后MMP表达增加的确切细胞信号通路;4)破坏依赖CADM1的HSC-3 细胞粘附是否增加了HSC-3 细胞的迁移和侵袭活性。结果:CADM1在LMF4细胞中的表达低于HSC-3 细胞。CADM1的敲除增加了HSC-3 细胞中MMP-2和MMP-9的表达。此外,CADM1敲除后MMP-2的表达上调被丝裂原活化蛋白(MAP)/细胞外信号调节激酶(MEK)抑制剂U0126和磷酸肌肽3-激酶(PI3K)抑制剂LY294002所消除。CADM1下调后MMP-9的表达上调被c-Jun n -末端激酶(JNK)抑制剂SP600125和p38 MAP激酶(MAPK)抑制剂SB203580和LY294002消除。抗cadm1中和抗体诱发HSC-3 细胞的迁移和侵袭能力。结论:人口腔鳞癌细胞中cadm1依赖性细胞-细胞粘附的破坏导致肿瘤进展,可能是通过MMP-2以MEK/ pi3k依赖性方式表达增加,MMP-9以JNK/p38 MAPK/ pi3k依赖性方式表达增加。
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引用次数: 0
Nano apatite growth on demineralized bone matrix capped with curcumin and silver nanoparticles: Dental implant mechanical stability and optimal cell growth analysis 姜黄素和银纳米颗粒覆盖的脱矿骨基质上的纳米磷灰石生长:牙科植入物机械稳定性和最佳细胞生长分析。
IF 2.4 Q2 Dentistry Pub Date : 2024-03-01 DOI: 10.1016/j.job.2023.12.004
Rethinam Senthil , Sinem Çakır

Objectives

The prevention of implant-associated infections is becoming increasingly clinically important in the field of dentistry. Extensive investigations into the development of innovative antibacterial materials that interact effectively to reinforce their functionality are currently being conducted in the biomedical sector. In the present study, a novel dental nano putty (D-nP) has been developed using demineralized bone matrix (DBM), calcium sulfate hemihydrate (CSH), curcumin nanoparticles (CU-NPs), and silver nanoparticles (AgNPs).

Methods

The produced D-nP was evaluated using physicochemical, mechanical, and in vitro analyses. Surface characterization, particularly the analysis of calcium and phosphorus content, was performed before and after immersion in the simulated body fluid (SBF). In addition, the impact of surface treatment on biological activity was studied.

Results

The results showed that the mechanical properties of the D-nP were outstanding and its performance is promising. D-nP exhibited excellent antibacterial activity against Actinomyces naeslundii (5.22 ± 0.07 mm) and Streptococcus oralis (5.41 ± 0.1 mm). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was conducted using MG-63 osteoblast cells, which exhibited 95 % viability in D-nP.

Conclusions

Based on these characterization results, the D-nP developed in this study exhibited excellent performance for tooth tissue in bone repair.

目的:在牙科领域,预防与种植体相关的感染正变得越来越重要。目前,生物医学领域正在广泛研究如何开发创新型抗菌材料,使其能够有效地相互作用以增强其功能。本研究使用去矿物质骨基质(DBM)、半水合硫酸钙(CSH)、姜黄素纳米颗粒(CU-NPs)和纳米银颗粒(AgNPs)开发了一种新型牙科纳米腻子(D-nP):通过理化、机械和体外分析对制备的 D-nP 进行了评估。在模拟体液(SBF)中浸泡前后进行了表面表征,特别是钙和磷含量分析。此外,还研究了表面处理对生物活性的影响:结果:研究结果表明,D-nP 的机械性能非常出色,性能前景广阔。D-nP 对放线菌(5.22 ± 0.07 mm)和口腔链球菌(5.41 ± 0.1 mm)具有出色的抗菌活性。使用 MG-63 成骨细胞进行了 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四氮唑(MTT)试验,结果表明 D-nP 具有 95% 的活力:根据这些表征结果,本研究中开发的 D-nP 在骨修复的牙组织中表现出卓越的性能。
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引用次数: 0
Oral biosciences: The annual review 2023 口腔生物科学:2023 年年度回顾。
IF 2.4 Q2 Dentistry Pub Date : 2024-03-01 DOI: 10.1016/j.job.2024.01.011
Hayato Ohshima , Kenji Mishima

Background

The Journal of Oral Biosciences is dedicated to advancing and disseminating fundamental knowledge with regard to every aspect of oral biosciences. This review features review articles in the fields of “bone regeneration,” “periodontitis,” “periodontal diseases,” “salivary glands,” “sleep bruxism,” and “Sjögren's syndrome.”

Highlight

This review focuses on human demineralized dentin and cementum matrices for bone regeneration, oxidized low-density lipoprotein in periodontal disease and systemic conditions, the relationship between inflammatory mediators in migraine and periodontitis, phosphoinositide signaling molecules in the salivary glands, and the pathophysiologies of sleep bruxism and Sjögren's syndrome.

Conclusion

The review articles featured in the Journal of Oral Biosciences have broadened the knowledge of readers regarding various aspects of oral biosciences. The current editorial review discusses the findings and significance of these review articles.

背景:口腔生物科学杂志》(Journal of Oral Biosciences)致力于推动和传播口腔生物科学各方面的基础知识。本综述主要介绍 "骨再生"、"牙周炎"、"牙周病"、"唾液腺"、"睡眠磨牙症 "和 "斯约格伦综合征 "等领域的综述文章:这篇综述主要关注人类脱矿化牙本质/骨灰基质促进骨再生、氧化低密度脂蛋白在牙周病和全身性疾病中的作用、偏头痛和牙周炎中炎症介质之间的关系、唾液腺中的磷脂酰肌醇信号分子以及睡眠磨牙症和斯约格伦综合征的病理生理学:口腔生物科学杂志》上的评论文章帮助读者拓宽了口腔生物科学各方面的知识。本期编辑评论将介绍这些精彩的评论文章。
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引用次数: 0
Supersulfides support bone growth by promoting chondrocyte proliferation in the growth plates 超硫化物通过促进生长板中的软骨细胞增殖来支持骨生长。
IF 2.4 Q2 Dentistry Pub Date : 2024-03-01 DOI: 10.1016/j.job.2023.11.004
Yuji Sasama , Kentaro Yoshimura , Marie Hoshino , Kiyohito Sasa , Takaaki Akaike , Masanobu Morita , Kazuyoshi Baba , Tatsuo Shirota , Yoichi Miyamoto

Objectives

While chondrocytes have mitochondria, they receive little O2 from the bloodstream. Sulfur respiration, an essential energy production system in mitochondria, uses supersulfides instead of O2. Supersulfides are inorganic and organic sulfides with catenated sulfur atoms and are primarily produced by cysteinyl tRNA synthetase-2 (CARS2). Here, we investigated the role of supersulfides in chondrocyte proliferation and bone growth driven by growth plate chondrocyte proliferation.

Methods

We examined the effects of NaHS, an HS/H2S donor, and cystine, the cellular source of cysteine, on the proliferation of mouse primary chondrocytes and growth of embryonic mouse tibia in vitro. We also examined the effect of RNA interference acting on the Cars2 gene on chondrocyte proliferation in the presence of cystine.

Results

NaHS (30 μmol/L) enhanced tibia longitudinal growth in vitro with expansion of the proliferating zone of their growth plates. While NaHS (30 μmol/L) also promoted chondrocyte proliferation only under normoxic conditions (20 % O2), cystine (0.5 mmol/L) promoted it under both normoxic and hypoxic (2 % O2) conditions. Cars2 gene knockdown abrogated the ability of cystine (0.5 mmol/L) to promote chondrocyte proliferation under normoxic conditions, indicating that supersulfides produced by CARS2 were responsible for the cystine-dependent promotion of bone growth.

Conclusions

The presented results indicate that supersulfides play a vital role in bone growth achieved by chondrocyte proliferation in the growth plates driven by sulfur respiration.

目的:虽然软骨细胞有线粒体,但它们从血液中获得的氧气很少。硫呼吸是线粒体中必不可少的能量生产系统,它使用超硫化物而不是O2。超硫化物是具有链化硫原子的无机和有机硫化物,主要由半胱氨酸tRNA合成酶2 (CARS2)产生。在这里,我们研究了超硫化物在软骨细胞增殖和生长板软骨细胞增殖驱动的骨生长中的作用。方法:研究了HS-/H2S供体NaHS和半胱氨酸细胞源半胱氨酸对小鼠原代软骨细胞增殖和胚胎胫骨体外生长的影响。我们还研究了在胱氨酸存在的情况下,RNA干扰作用于Cars2基因对软骨细胞增殖的影响。结果:NaHS(30 μmol/L)能促进胫骨纵向生长,使生长板增殖带扩大。NaHS(30 μmol/L)仅在常氧(20 % O2)条件下促进软骨细胞增殖,而胱氨酸(0.5 mmol/L)在常氧和缺氧(2 % O2)条件下均促进软骨细胞增殖。在常氧条件下,Cars2基因敲低使胱氨酸(0.5 mmol/L)促进软骨细胞增殖的能力丧失,表明Cars2产生的超硫化物是胱氨酸依赖性促进骨生长的原因。结论:本研究结果表明,超硫化物在硫呼吸驱动的生长板中通过软骨细胞增殖实现骨生长中起重要作用。
{"title":"Supersulfides support bone growth by promoting chondrocyte proliferation in the growth plates","authors":"Yuji Sasama ,&nbsp;Kentaro Yoshimura ,&nbsp;Marie Hoshino ,&nbsp;Kiyohito Sasa ,&nbsp;Takaaki Akaike ,&nbsp;Masanobu Morita ,&nbsp;Kazuyoshi Baba ,&nbsp;Tatsuo Shirota ,&nbsp;Yoichi Miyamoto","doi":"10.1016/j.job.2023.11.004","DOIUrl":"10.1016/j.job.2023.11.004","url":null,"abstract":"<div><h3>Objectives</h3><p>While chondrocytes have mitochondria, they receive little O<sub>2</sub> from the bloodstream. Sulfur respiration, an essential energy production system in mitochondria, uses supersulfides instead of O<sub>2</sub>. Supersulfides are inorganic and organic sulfides with catenated sulfur atoms and are primarily produced by cysteinyl tRNA synthetase-2 (CARS2). Here, we investigated the role of supersulfides in chondrocyte proliferation and bone growth driven by growth plate chondrocyte proliferation.</p></div><div><h3>Methods</h3><p>We examined the effects of NaHS, an HS<sup>−</sup>/H<sub>2</sub>S donor, and cystine, the cellular source of cysteine, on the proliferation of mouse primary chondrocytes and growth of embryonic mouse tibia <em>in vitro</em>. We also examined the effect of RNA interference acting on the <em>Cars2</em> gene on chondrocyte proliferation in the presence of cystine.</p></div><div><h3>Results</h3><p>NaHS (30 μmol/L) enhanced tibia longitudinal growth <em>in vitro</em> with expansion of the proliferating zone of their growth plates. While NaHS (30 μmol/L) also promoted chondrocyte proliferation only under normoxic conditions (20 % O<sub>2</sub>), cystine (0.5 mmol/L) promoted it under both normoxic and hypoxic (2 % O<sub>2</sub>) conditions. <em>Cars2</em> gene knockdown abrogated the ability of cystine (0.5 mmol/L) to promote chondrocyte proliferation under normoxic conditions, indicating that supersulfides produced by CARS2 were responsible for the cystine-dependent promotion of bone growth.</p></div><div><h3>Conclusions</h3><p>The presented results indicate that supersulfides play a vital role in bone growth achieved by chondrocyte proliferation in the growth plates driven by sulfur respiration.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007923001858/pdfft?md5=3d9e86f8aa406e3b48a1390d11fac056&pid=1-s2.0-S1349007923001858-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138048168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
PAR2-dependent phosphorylation of TRPV4 at the trigeminal nerve terminals contributes to tongue cancer pain 三叉神经末梢TRPV4的PAR2依赖性磷酸化导致舌癌症疼痛。
IF 2.4 Q2 Dentistry Pub Date : 2023-10-12 DOI: 10.1016/j.job.2023.10.003
Ryuta Akasaka , Akihiko Furukawa , Yoshinori Hayashi , Suzuro Hitomi , Ryo Koyama , Eri Oshima , Miki Tamura , Mamiko Yonemoto , Yasushi Hojo , Ryosuke Takahashi , Ikuko Shibuta , Koichi Iwata , Yoshiyuki Yonehara , Masamichi Shinoda

Objective

This study aimed to clarify the interactions between the tongue and primary afferent fibers in tongue cancer pain.

Methods

A pharmacological analysis was conducted to evaluate mechanical hypersensitivity of the tongues of rats with squamous cell carcinoma (SCC). Changes in trigeminal ganglion (TG) neurons projecting to the tongue were analyzed using immunohistochemistry and western blotting.

Results

SCC inoculation of the tongue caused persistent mechanical sensitization and tumor formation. Trypsin expression was significantly upregulated in cancer lesions. Continuous trypsin inhibition or protease-activated receptor 2 (PAR2) antagonism in the tongue significantly inhibited SCC-induced mechanical sensitization. No changes were observed in PAR2 and transient receptor potential vanilloid 4 (TRPV4) levels in the TG or the number of PAR2-and TRPV4-expressing TG neurons after SCC inoculation. In contrast, the relative amount of phosphorylated TRPV4 in the TG was significantly increased after SCC inoculation and abrogated by PAR2 antagonism in the tongue. TRPV4 antagonism in the tongue significantly ameliorated the mechanical sensitization caused by SCC inoculation.

Conclusions

Our findings indicate that tumor-derived trypsin sensitizes primary afferent fibers by PAR2 stimulation and subsequent TRPV4 phosphorylation, resulting in severe tongue pain.

目的:本研究旨在阐明舌与初级传入纤维在舌癌症疼痛中的相互作用。方法:采用药理学方法评价大鼠舌鳞状细胞癌(SCC)的机械性超敏反应。用免疫组织化学和蛋白质印迹法分析了投射到舌头的三叉神经节(TG)神经元的变化。结果:SCC接种引起舌部持续的机械致敏和肿瘤形成。在癌症病变中胰蛋白酶表达显著上调。舌头中持续的胰蛋白酶抑制或蛋白酶激活受体2(PAR2)拮抗作用显著抑制SCC诱导的机械致敏。SCC接种后,TG中的PAR2和瞬时受体电位香草素4(TRPV4)水平或表达PAR2和TRPV4的TG神经元的数量没有变化。相反,SCC接种后TG中磷酸化TRPV4的相对量显著增加,并被舌头中的PAR2拮抗作用消除。TRPV4在舌头中的拮抗作用显著改善了SCC接种引起的机械致敏。结论:我们的研究结果表明,肿瘤来源的胰蛋白酶通过PAR2刺激和随后的TRPV4磷酸化使初级传入纤维增敏,导致严重的舌痛。
{"title":"PAR2-dependent phosphorylation of TRPV4 at the trigeminal nerve terminals contributes to tongue cancer pain","authors":"Ryuta Akasaka ,&nbsp;Akihiko Furukawa ,&nbsp;Yoshinori Hayashi ,&nbsp;Suzuro Hitomi ,&nbsp;Ryo Koyama ,&nbsp;Eri Oshima ,&nbsp;Miki Tamura ,&nbsp;Mamiko Yonemoto ,&nbsp;Yasushi Hojo ,&nbsp;Ryosuke Takahashi ,&nbsp;Ikuko Shibuta ,&nbsp;Koichi Iwata ,&nbsp;Yoshiyuki Yonehara ,&nbsp;Masamichi Shinoda","doi":"10.1016/j.job.2023.10.003","DOIUrl":"10.1016/j.job.2023.10.003","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to clarify the interactions between the tongue and primary afferent fibers in tongue cancer pain.</p></div><div><h3>Methods</h3><p>A pharmacological analysis was conducted to evaluate mechanical hypersensitivity<span><span> of the tongues of rats with squamous cell carcinoma (SCC). Changes in trigeminal ganglion (TG) neurons projecting to the tongue were analyzed using </span>immunohistochemistry<span> and western blotting.</span></span></p></div><div><h3>Results</h3><p>SCC inoculation of the tongue caused persistent mechanical sensitization and tumor formation. Trypsin expression was significantly upregulated in cancer lesions. Continuous trypsin inhibition<span> or protease-activated receptor 2 (PAR2) antagonism in the tongue significantly inhibited SCC-induced mechanical sensitization. No changes were observed in PAR2 and transient receptor potential vanilloid 4 (TRPV4) levels in the TG or the number of PAR2-and TRPV4-expressing TG neurons after SCC inoculation. In contrast, the relative amount of phosphorylated TRPV4 in the TG was significantly increased after SCC inoculation and abrogated by PAR2 antagonism in the tongue. TRPV4 antagonism in the tongue significantly ameliorated the mechanical sensitization caused by SCC inoculation.</span></p></div><div><h3>Conclusions</h3><p>Our findings indicate that tumor-derived trypsin sensitizes primary afferent fibers by PAR2 stimulation and subsequent TRPV4 phosphorylation, resulting in severe tongue pain.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41215668","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
Alcohol consumption modulates Candida albicans-induced oral carcinogenesis and progression 饮酒可调节白色念珠菌引起的口腔癌变和进展。
IF 2.4 Q2 Dentistry Pub Date : 2023-10-06 DOI: 10.1016/j.job.2023.10.002
Isabel O'Grady, Jeff O'Sullivan

Objectives

This study aimed to determine the impact of low levels of alcohol consumption on the interaction of the oral cavity with Candida albicans, a species that is commonly found at higher levels in the oral cavities of regular alcohol consumers, patients with pre-malignant diseases, and patients with existing oral cancer (OC).

Methods

The gingival squamous cell carcinoma cell line, Ca9-22, was subjected to low-level ethanol exposure before co-culture with heat-inactivated C. albicans (HICA). We performed cell viability assays, measured reactive oxygen species, and used Western blot analysis for cell death markers to examine the effect of ethanol and HICA on cells. Scratch assays and anchorage-independent growth assays were used to determine cell behavioral changes.

Results

The results showed that ethanol in combination with HICA exacerbated cell death and cell cycle disruption, delayed NF-κB signaling, increased TIMP-2 secretion, and subsequently decreased MMP-2 secretion when compared to exposure to HICA alone. Conversely, both ethanol and HICA independently increased proliferation of Ca9-22 cells in scratch assays, and in combination, increased their capacity for anchorage-independent growth.

Conclusion

Low levels of ethanol may provide protective effects against Candida-induced inflammatory oral carcinogenesis or OC progression.

目的:本研究旨在确定低水平饮酒对口腔与白色念珠菌相互作用的影响,白色念珠菌是一种常见于正常饮酒者、恶性疾病前患者和现有口腔癌症(OC)患者口腔中较高水平的白色念珠菌,在与热灭活的白色念珠菌(HICA)共培养之前进行低水平乙醇暴露。我们进行了细胞活力测定,测量了活性氧,并使用细胞死亡标志物的蛋白质印迹分析来检测乙醇和HICA对细胞的影响。使用划痕试验和锚定无关生长试验来确定细胞行为变化。结果:与单独暴露于HICA相比,乙醇与HICA联合使用会加剧细胞死亡和细胞周期破坏,延迟NF-κB信号传导,增加TIMP-2分泌,随后减少MMP-2分泌。相反,在划痕试验中,乙醇和HICA都独立地增加了Ca9-22细胞的增殖,并联合增加了其锚定非依赖性生长的能力。结论:低水平的乙醇可能对念珠菌诱导的炎症性口腔癌变或OC进展具有保护作用。
{"title":"Alcohol consumption modulates Candida albicans-induced oral carcinogenesis and progression","authors":"Isabel O'Grady,&nbsp;Jeff O'Sullivan","doi":"10.1016/j.job.2023.10.002","DOIUrl":"10.1016/j.job.2023.10.002","url":null,"abstract":"<div><h3>Objectives</h3><p><span>This study aimed to determine the impact of low levels of alcohol consumption on the interaction of the oral cavity with </span><span><em>Candida albicans</em></span>, a species that is commonly found at higher levels in the oral cavities of regular alcohol consumers, patients with pre-malignant diseases, and patients with existing oral cancer (OC).</p></div><div><h3>Methods</h3><p>The gingival squamous cell carcinoma cell line, Ca9-22, was subjected to low-level ethanol exposure before co-culture with heat-inactivated <em>C. albicans</em><span><span><span><span> (HICA). We performed cell viability assays, measured </span>reactive oxygen species, and used </span>Western blot analysis for </span>cell death<span> markers to examine the effect of ethanol and HICA on cells. Scratch assays and anchorage-independent growth assays were used to determine cell behavioral changes.</span></span></p></div><div><h3>Results</h3><p>The results showed that ethanol in combination with HICA exacerbated cell death and cell cycle disruption, delayed NF-κB signaling, increased TIMP-2 secretion, and subsequently decreased MMP-2 secretion when compared to exposure to HICA alone. Conversely, both ethanol and HICA independently increased proliferation of Ca9-22 cells in scratch assays, and in combination, increased their capacity for anchorage-independent growth.</p></div><div><h3>Conclusion</h3><p>Low levels of ethanol may provide protective effects against <em>Candida</em>-induced inflammatory oral carcinogenesis or OC progression.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41152010","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
Curcumin attenuates replicative senescence in human dental follicle cells and restores their osteogenic differentiation 姜黄素可减轻人类牙毛囊细胞的复制性衰老,并恢复其成骨分化。
IF 2.4 Q2 Dentistry Pub Date : 2023-10-06 DOI: 10.1016/j.job.2023.10.001
Divyamaanasa Dasi , Nayudu Nallabelli , Ravisankar Devalaraju , Sushma K N , Sudip Ghosh , Roy Karnati , Pasupuleti Sreenivasa Rao

Objective

This study aimed to examine the therapeutic effects of curcumin against replicative senescence in dental follicle cells (DFCs).

Methods

Human DFCs were cultured in Dulbecco's Modified Eagle Medium with growth supplements. Replicative senescence in DFCs at different passages was assessed using β-galactosidase activity assay. Cell proliferation and size of DFCs at different passages were determined by CCK-8 kit and microscopy method, respectively. In addition, curcumin's effect on replicative senescence, cell proliferation, and size of DFCs at different passages was analyzed. Using western-blot analysis and siRNA-mediated gene silencing, we determined the molecular mechanisms involved in curcumin's effect against replicative senescence and osteogenic differentiation in DFCs at different passages.

Results

We observed decreased proliferation and increased cell size and replicative senescence in cultured human DFCs at higher passages. Intriguingly, despite not showing any effect on cell size, curcumin (50 μM) significantly restored proliferation ability in DFCs and inhibited their replicative senescence. Concerning mechanisms, we found that curcumin inhibits replicative senescence in DFCs via down-regulation of senescence markers (P16 & P21) and restoration of proliferation markers (E2F1 & P53). Additionally, curcumin also rescued the osteogenic differentiation potential in higher-passage DFCs via restoration of osteogenic markers RUNX2 and OPN.

Conclusion

Our findings reveal for the first time that curcumin could act as a potential anti-senescence therapeutic for DFCs via regulation of proliferation, senescence, and osteogenic differentiation markers.

目的:本研究旨在检测姜黄素对牙毛囊细胞(DFCs)复制性衰老的治疗作用。方法:在添加生长补充剂的Dulbecco改良Eagle培养基中培养人DFCs。用β-半乳糖苷酶活性测定法评估DFCs在不同传代期的复制衰老。分别用CCK-8试剂盒和显微镜法测定不同传代期DFCs的增殖和大小。此外,还分析了姜黄素对不同传代的复制衰老、细胞增殖和DFCs大小的影响。利用蛋白质印迹分析和siRNA介导的基因沉默,我们确定了姜黄素在不同传代中对抗DFCs复制衰老和成骨分化的分子机制。结果:我们观察到培养的人DFCs在较高传代时增殖减少,细胞大小增加,复制衰老。有趣的是,尽管姜黄素(50μM)对细胞大小没有任何影响,但它显著恢复了DFCs的增殖能力,并抑制了其复制衰老。关于机制,我们发现姜黄素通过下调衰老标志物(P16和P21)和恢复增殖标志物(E2F1和P53)来抑制DFCs的复制性衰老。此外,姜黄素还通过恢复成骨标志物RUNX2和OPN,挽救了高传代DFCs的成骨分化潜力。结论:我们的研究结果首次表明,姜黄素可以通过调节增殖、衰老和成骨分化标志物,对DFCs起到潜在的抗衰老治疗作用。
{"title":"Curcumin attenuates replicative senescence in human dental follicle cells and restores their osteogenic differentiation","authors":"Divyamaanasa Dasi ,&nbsp;Nayudu Nallabelli ,&nbsp;Ravisankar Devalaraju ,&nbsp;Sushma K N ,&nbsp;Sudip Ghosh ,&nbsp;Roy Karnati ,&nbsp;Pasupuleti Sreenivasa Rao","doi":"10.1016/j.job.2023.10.001","DOIUrl":"10.1016/j.job.2023.10.001","url":null,"abstract":"<div><h3>Objective</h3><p><span>This study aimed to examine the therapeutic effects of curcumin against replicative senescence in </span>dental follicle cells (DFCs).</p></div><div><h3>Methods</h3><p>Human DFCs were cultured in Dulbecco's Modified Eagle Medium with growth supplements. Replicative senescence in DFCs at different passages was assessed using β-galactosidase activity assay. Cell proliferation<span> and size of DFCs at different passages were determined by CCK-8 kit and microscopy method, respectively. In addition, curcumin's effect on replicative senescence, cell proliferation, and size of DFCs at different passages was analyzed. Using western-blot analysis and siRNA-mediated gene silencing, we determined the molecular mechanisms involved in curcumin's effect against replicative senescence and osteogenic differentiation in DFCs at different passages.</span></p></div><div><h3>Results</h3><p><span>We observed decreased proliferation and increased cell size and replicative senescence in cultured human DFCs at higher passages. Intriguingly, despite not showing any effect on cell size, curcumin (50 μM) significantly restored proliferation ability in DFCs and inhibited their replicative senescence. Concerning mechanisms, we found that curcumin inhibits replicative senescence in DFCs via down-regulation of senescence markers (P16 &amp; P21) and restoration of proliferation markers (E2F1 &amp; P53). Additionally, curcumin also rescued the osteogenic differentiation potential in higher-passage DFCs via restoration of osteogenic markers </span>RUNX2<span> and OPN.</span></p></div><div><h3>Conclusion</h3><p>Our findings reveal for the first time that curcumin could act as a potential anti-senescence therapeutic for DFCs via regulation of proliferation, senescence, and osteogenic differentiation markers.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41137290","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
Fundamental research for dose control during supine dental panoramic radiography 仰卧位牙科全景x线摄影剂量控制的基础研究。
IF 2.4 Q2 Dentistry Pub Date : 2023-09-17 DOI: 10.1016/j.job.2023.09.003
Atsuharu Nitanda , Atsushi Iwawaki , Yusei Otaka , Yuichi Tamatsu , Takeru Ishii , Akihiro Ochiai , Yuko Otomo , Shinji Kito , Hideki Saka

Objective

This study aimed to control radiation doses when using a portable supine dental panoramic radiography system by measured the scattered doses.

Method

The study used LPX7007 (Asahi Roentgen) for the panoramic radiography system. The subjects comprised a cylinder phantom (QualitA) and a RANDO Phantom (Alderson). The semiconductor dosimeter was an X2 survey sensor (RaySafe). The phantom was set at a height of 1 m from the floor, and the sensor was set at 1 m from the floor at the genital level and 1.5 m at the lens level. Measurements were taken at 30°intervals clockwise from 0°at distances of 0.5 m and 1 m in radius around the phantom. The occupational exposure range was defined as 0 ± 30° and the public exposure range was defined as the occupational exposure range and 30° to 150° and 210° to 330° as the public exposure range.

Result

The highest doses were observed in the 120° and 240° directions, and the lowest in 0° ± 30° range. The lowest limit number of images taken in the occupational exposure range was 130 images at a distance of 0.5 m, 452 images at 1 m at the lens level for the cylinder phantom, and 320 images at 0.5 m and 1098 images at 1 m for the RANDO Phantom. In the public exposure range at the genital level, there was one image at 0.5 m and six images at 1 m for the cylinder phantom, and two images at 0.5 m and eight images at 1 m for the RANDO Phantom.

Conclusion

We found that radiation exposure can be reduced by keeping a distance from the subject, avoiding working at 120° and 240° and staying within 0° ± 30° behind the panoramic radiography system.

目的:通过测量分散剂量来控制便携式仰卧牙科全景x线摄影系统使用时的辐射剂量。方法:采用LPX7007(旭伦琴)作为全景摄影系统。受试者包括一个圆柱体幻影(QualitA)和一个随机幻影(Alderson)。半导体剂量计为X2测量传感器(RaySafe)。幻影被设置在离地面1米的高度,传感器被设置在离地面1米的生殖器水平和离地面1.5米的镜头水平。测量从0°开始顺时针间隔30°,距离为0.5 m和1 m。职业暴露范围定义为0±30°,公共暴露范围定义为职业暴露范围,公共暴露范围定义为30°~ 150°和210°~ 330°。结果:120°和240°方向剂量最高,0°±30°范围剂量最低。在职业曝光范围内拍摄的最低限制图像数量为:在0.5 m距离处拍摄130张图像,圆柱体幻影在1 m距离处拍摄452张图像,RANDO幻影在0.5 m距离处拍摄320张图像,在1 m距离处拍摄1098张图像。在生殖器水平的公共暴露范围内,圆柱体幻影在0.5 m处有1幅图像,在1 m处有6幅图像,RANDO幻影在0.5 m处有2幅图像,在1 m处有8幅图像。结论:与被摄体保持一定距离,避免在120°和240°的角度工作,并保持在全景摄影系统后方0°±30°范围内,可以减少辐射暴露。
{"title":"Fundamental research for dose control during supine dental panoramic radiography","authors":"Atsuharu Nitanda ,&nbsp;Atsushi Iwawaki ,&nbsp;Yusei Otaka ,&nbsp;Yuichi Tamatsu ,&nbsp;Takeru Ishii ,&nbsp;Akihiro Ochiai ,&nbsp;Yuko Otomo ,&nbsp;Shinji Kito ,&nbsp;Hideki Saka","doi":"10.1016/j.job.2023.09.003","DOIUrl":"10.1016/j.job.2023.09.003","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to control radiation doses when using a portable supine dental panoramic radiography system by measured the scattered doses.</p></div><div><h3>Method</h3><p>The study used LPX7007 (Asahi Roentgen) for the panoramic radiography system. The subjects comprised a cylinder phantom (QualitA) and a RANDO Phantom (Alderson). The semiconductor dosimeter was an X2 survey sensor (RaySafe). The phantom was set at a height of 1 m from the floor, and the sensor was set at 1 m from the floor at the genital level and 1.5 m at the lens level. Measurements were taken at 30°intervals clockwise from 0°at distances of 0.5 m and 1 m in radius around the phantom. The occupational exposure range was defined as 0 ± 30° and the public exposure range was defined as the occupational exposure range and 30° to 150° and 210° to 330° as the public exposure range.</p></div><div><h3>Result</h3><p>The highest doses were observed in the 120° and 240° directions, and the lowest in 0° ± 30° range. The lowest limit number of images taken in the occupational exposure range was 130 images at a distance of 0.5 m, 452 images at 1 m at the lens level for the cylinder phantom, and 320 images at 0.5 m and 1098 images at 1 m for the RANDO Phantom. In the public exposure range at the genital level, there was one image at 0.5 m and six images at 1 m for the cylinder phantom, and two images at 0.5 m and eight images at 1 m for the RANDO Phantom.</p></div><div><h3>Conclusion</h3><p>We found that radiation exposure can be reduced by keeping a distance from the subject, avoiding working at 120° and 240° and staying within 0° ± 30° behind the panoramic radiography system.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10634076","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
DKK3 expression is correlated with poorer prognosis in head and neck squamous cell carcinoma: A bioinformatics study based on the TCGA database DKK3表达与头颈部鳞状细胞癌预后不良相关:基于TCGA数据库的生物信息学研究
IF 2.4 Q2 Dentistry Pub Date : 2023-09-15 DOI: 10.1016/j.job.2023.09.002
Naoki Katase , Shin-ichiro Nishimatsu , Akira Yamauchi , Shinji Okano , Shuichi Fujita

Objective

We previously reported that dickkopf WNT signaling pathway inhibitor 3 (DKK3) expression is correlated with poorer prognosis in head and neck squamous cell carcinoma (HNSCC). Here we investigated DKK3 expression by using The Cancer Genome Atlas (TCGA) public database and bioinformatic analyses.

Methods

We used the RNA sequence data and divided the tumor samples into “DKK3-high” and “DKK3-low” groups according to median DKK3 expression. The correlations between DKK3 expression and the clinical data were investigated. Differentially expressed genes (DEGs) were detected using DESEq2 and analyzed by ShinyGO 0.77. A gene set enrichment analysis (GSEA) was also performed using GSEA software. The DEGs were also analyzed with TargetMine to establish the protein–protein interaction (PPI) network.

Results

DKK3 expression was significantly increased in cancer samples, and a high DKK3 expression was significantly associated with shorter overall survival. We identified 854 DEGs, including 284 up-regulated and 570 down-regulated. Functional enrichment analyses revealed several Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with extracellular matrix remodeling. The PPI network identified COL8A1, AGTR1, FN1, P4HA3, PDGFRB, and CEP126 as the key genes.

Conclusions

These results suggested the cancer-promoting ability of DKK3, the expression of which is a promising prognostic marker and therapeutic target for HNSCC.

目的:我们之前报道dickkopf WNT信号通路抑制剂3 (DKK3)表达与头颈部鳞状细胞癌(HNSCC)预后不良相关。本研究利用癌症基因组图谱(TCGA)公共数据库和生物信息学分析来研究DKK3的表达。方法:利用RNA序列数据,根据DKK3中位表达水平将肿瘤样本分为“DKK3高”组和“DKK3低”组。探讨DKK3表达与临床数据的相关性。用DESEq2检测差异表达基因(DEGs),用ShinyGO 0.77分析差异表达基因(DEGs)。使用GSEA软件进行基因集富集分析(GSEA)。用TargetMine软件分析这些基因,建立蛋白-蛋白相互作用(PPI)网络。结果:肿瘤样本中DKK3表达显著升高,且DKK3高表达与总生存期缩短显著相关。共鉴定出854个基因,其中284个基因上调,570个基因下调。功能富集分析揭示了几个与细胞外基质重塑相关的基因本体(GO)术语和京都基因与基因组百科全书(KEGG)途径。PPI网络鉴定出COL8A1、AGTR1、FN1、P4HA3、PDGFRB和CEP126为关键基因。结论:这些结果提示DKK3具有促癌能力,其表达是HNSCC有希望的预后标志物和治疗靶点。
{"title":"DKK3 expression is correlated with poorer prognosis in head and neck squamous cell carcinoma: A bioinformatics study based on the TCGA database","authors":"Naoki Katase ,&nbsp;Shin-ichiro Nishimatsu ,&nbsp;Akira Yamauchi ,&nbsp;Shinji Okano ,&nbsp;Shuichi Fujita","doi":"10.1016/j.job.2023.09.002","DOIUrl":"10.1016/j.job.2023.09.002","url":null,"abstract":"<div><h3>Objective</h3><p><span>We previously reported that dickkopf WNT signaling pathway inhibitor 3 (</span><em>DKK3</em><span>) expression is correlated with poorer prognosis in head and neck squamous cell carcinoma (HNSCC). Here we investigated </span><em>DKK3</em><span> expression by using The Cancer Genome Atlas (TCGA) public database and bioinformatic analyses.</span></p></div><div><h3>Methods</h3><p><span>We used the RNA sequence data and divided the tumor samples into “</span><em>DKK3</em>-high” and “<em>DKK3</em>-low” groups according to median <em>DKK3</em> expression. The correlations between <em>DKK3</em><span> expression and the clinical data were investigated. Differentially expressed genes (DEGs) were detected using DESEq2 and analyzed by ShinyGO 0.77. A gene set enrichment analysis (GSEA) was also performed using GSEA software. The DEGs were also analyzed with TargetMine to establish the protein–protein interaction (PPI) network.</span></p></div><div><h3>Results</h3><p><em>DKK3</em> expression was significantly increased in cancer samples, and a high <em>DKK3</em><span><span> expression was significantly associated with shorter overall survival. We identified 854 DEGs, including 284 up-regulated and 570 down-regulated. Functional enrichment analyses revealed several Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with </span>extracellular matrix remodeling. The PPI network identified </span><em>COL8A1</em>, <em>AGTR1</em>, <em>FN1</em>, <em>P4HA3</em>, <span><em>PDGFRB</em><em>,</em></span> and <em>CEP126</em> as the key genes.</p></div><div><h3>Conclusions</h3><p>These results suggested the cancer-promoting ability of <em>DKK3</em>, the expression of which is a promising prognostic marker and therapeutic target for HNSCC.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10273447","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
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Journal of Oral Biosciences
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