Journal of Oral Biosciences最新文献

{"title":"Proinflammatory cytokine-induced matrix metalloproteinase-9 expression in temporomandibular joint osteoarthritis is regulated by multiple intracellular mitogen-activated protein kinase pathways","authors":"Karen Abe ,&nbsp;Seiji Yokota ,&nbsp;Shikino Matsumoto ,&nbsp;Hayato Ujiie ,&nbsp;Emiko Kikuchi ,&nbsp;Kazuro Satoh ,&nbsp;Akira Ishisaki ,&nbsp;Naoyuki Chosa","doi":"10.1016/j.job.2024.100609","DOIUrl":"10.1016/j.job.2024.100609","url":null,"abstract":"<div><h3>Objectives</h3><div>Temporomandibular joint (TMJ) osteoarthritis (OA) is an inflammatory disease that involves periarthritis of the TMJ and destruction of cartilage tissue in the mandibular condyle. However, the role of proinflammatory cytokines in the expression levels of matrix metalloproteinase (MMP) remains inconclusive. Thus, in this study, we aimed to investigate the effect of proinflammatory cytokines on the expression of MMPs.</div></div><div><h3>Methods</h3><div>FLS1 cells (mouse TMJ-derived synovial cell line) were treated with tumor necrosis factor alpha (TNF-α) or interleukin (IL)-1β in the presence or absence of mitogen-activated protein kinase (MAPK) inhibitors. The mRNA expression levels of MMP-2 and MMP-9 were examined by reverse transcription-quantitative polymerase chain reaction. Additionally, the phosphorylation status of extracellular signal-regulated kinase (ERK)1/2 and p38 MAPK in the FLS1 cells treated with TNF-α or IL-1β was evaluated by performing western blotting analysis.</div></div><div><h3>Results</h3><div>TNF-α and IL-1β significantly increased the expression of MMP-9 in the FLS1 cells; however, MMP-2 expression remained unaffected. Mitogen-activated protein kinase kinase (MEK) and p38 MAPK inhibitors significantly suppressed cytokine-induced MMP-9 upregulation. Conversely, Jun amino-terminal kinase (JNK) inhibitors further increased MMP-9 expression in the cells treated with TNF-α or IL-1β. Moreover, TNF-α and IL-1β enhanced ERK1/2 and p38 MAPK phosphorylation in the FLS1 cells.</div></div><div><h3>Conclusions</h3><div>TNF-α and IL-1β induced MMP-9 expression in the FLS1 cells via the MEK/ERK and p38 MAPK pathways and suppressed it via the JNK pathway. Thus, proinflammatory cytokines control MMP-9 expression in TMJ-OA by regulating multiple MAPK pathways.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100609"},"PeriodicalIF":2.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928232","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}

{"title":"Possible role of superoxide dismutase 3 in hypoxia-induced developmental defects in murine molars","authors":"Yeming Lu,&nbsp;Yukiho Kobayashi,&nbsp;Yuki Niki,&nbsp;Keiji Moriyama","doi":"10.1016/j.job.2024.100611","DOIUrl":"10.1016/j.job.2024.100611","url":null,"abstract":"<div><h3>Objectives</h3><div>To investigate the effects of hypoxia on tooth germ development in mice and explore the underlying mechanisms.</div></div><div><h3>Methods</h3><div>Tooth germs were extracted from E14.5 mouse embryos and divided into the control and hypoxia groups for organ culture. The hypoxia group was exposed to hypoxia (0% oxygen) for 3 h, followed by normoxia for 21 h. After 2 or 7 days, samples were collected for morphometric analysis, reverse transcription-quantitative polymerase chain reaction, immunohistochemistry (IHC), and immunofluorescent staining (IF). Additionally, superoxide dismutase 3 (SOD3) expression patterns in mandibular molar tooth germs from C57BL/6 mouse embryos were analyzed using IHC. The SOD inhibitor sodium N, N-diethyldithiocarbamate trihydrate (DETC; 400 μM) was applied under normoxia for 3 days, followed by morphometry, IHC, and IF.</div></div><div><h3>Results</h3><div>After 7 days, the hypoxia group exhibited significantly smaller tooth size, fewer cusps, reduced cell proliferation, and increased apoptosis in the epithelium compared to the control group. <em>Sod3</em> mRNA expression was higher than other <em>Sod</em> family member expressions in the control group. In the hypoxia group, <em>Sod3</em> mRNA and SOD3 protein expression were significantly decreased, whereas hypoxia-inducible factor-1 expression and reactive oxygen species levels were increased. SOD3 was primarily expressed in the dental epithelium from E12.5 to E17.5. DETC impaired tooth germ development in the control group, resulting in a phenotype similar to that of the hypoxia group, and significantly reduced amelogenin and msh homeobox 2 expression in the epithelium.</div></div><div><h3>Conclusions</h3><div>Hypoxia impairs tooth germ development. SOD3 probably plays a protective role during this process.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100611"},"PeriodicalIF":2.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923314","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}

{"title":"Characterization of the anti-Porphyromonas gingivalis compound in bilberry (Vaccinium myrtillus L.) and comparison with its analogs","authors":"Yutaroh Satoh ,&nbsp;Kazuyuki Ishihara ,&nbsp;Takaaki Kubota","doi":"10.1016/j.job.2024.100610","DOIUrl":"10.1016/j.job.2024.100610","url":null,"abstract":"<div><h3>Objectives</h3><div>The bacterium <em>Porphyromonas gingivalis</em> is a major causative agent of periodontitis. In this study, the anti-<em>P. gingivalis</em> compound in bilberry (<em>Vaccinium myrtillus</em> L.) was identified and its activity was compared with that of its related analogs.</div></div><div><h3>Methods</h3><div>An acetone-soluble bilberry fruit extract was purified using silica gel column chromatography, and the minimum inhibitory concentrations (MICs) of the purified fractions were determined against <em>P. gingivalis</em>. After purification, mass spectrometry, nuclear magnetic resonance, and optical rotation analyses were performed to identify the anti-<em>P. gingivalis</em> compounds. Furthermore, cell assays were performed to assess the anti-<em>P. gingivalis</em> activity and cytotoxicity of the identified compounds. The activity of these compounds was compared with that of their pentacyclic triterpene analogs.</div></div><div><h3>Results</h3><div>The anti-<em>P. gingivalis</em> in bilberry extracts was identified as ursolic acid, a pentacyclic triterpene (PCT). The MIC of ursolic acid against <em>P. gingivalis</em> was between 6.25 and 12.5 μg/mL; it killed <em>P. gingivalis</em> within 4 h of treatment at these concentrations. However, it showed no cytotoxicity against gingival carcinoma Ca9-22 cells at the MIC. Ursane-type PCT, including ursolic acid and oleanane-type PCT, exhibited anti-<em>P. gingivalis</em> activity.</div></div><div><h3>Conclusions</h3><div>Ursolic acid found in bilberry fruit extract exhibits anti-<em>P. gingivalis</em> activity. Similar activity is observed in a class of PCTs with a common structure.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100610"},"PeriodicalIF":2.6,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923311","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}

{"title":"Profiling of the microbes on the surface of smartphone touchscreens","authors":"Nanase Takahashi ,&nbsp;Anna Wakui ,&nbsp;Yume Sekizawa ,&nbsp;Miho Kawachi ,&nbsp;Mirai Sekiguchi ,&nbsp;Takashi Abe ,&nbsp;Aya Sato ,&nbsp;Misato Miyazawa ,&nbsp;Manami Imai ,&nbsp;Nagara Kaku ,&nbsp;Shingo Maruyama ,&nbsp;Hiroto Sano ,&nbsp;Nahoko Kakihara ,&nbsp;Jumpei Washio ,&nbsp;Yuki Abiko ,&nbsp;Kaori Tanaka ,&nbsp;Nobuhiro Takahashi ,&nbsp;Takuichi Sato","doi":"10.1016/j.job.2024.100607","DOIUrl":"10.1016/j.job.2024.100607","url":null,"abstract":"<div><div>The commensal microbiota of the finger-skin before and after ethanol disinfection were characterized and compared with the microbes isolated from the surface of smartphone touchscreens. The number of bacteria on the smartphone touchscreens was low, similar to that on the fingers after ethanol disinfection, suggesting that the surface of the touchscreens may not be suitable for the growth of microorganisms, rather than the surface of the fingers. Furthermore, ethanol disinfection reduced the number of bacteria on the finger-skin to 1/13 of the original count before disinfection.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100607"},"PeriodicalIF":2.6,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915892","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}

{"title":"Tooth loss-associated neuroplasticity of mastication-related motor cortical neurons","authors":"Takafumi Katagiri ,&nbsp;Shiro Nakamura ,&nbsp;Yoshihisa Tachibana ,&nbsp;Kiyomi Nakayama ,&nbsp;Ayako Mochizuki ,&nbsp;Masanori Dantsuji ,&nbsp;Kazuyoshi Baba ,&nbsp;Tomio Inoue","doi":"10.1016/j.job.2024.100606","DOIUrl":"10.1016/j.job.2024.100606","url":null,"abstract":"<div><h3>Objectives</h3><div>The cerebral cortex contains neurons that play a pivotal role in controlling rhythmic masticatory jaw movements. However, the population characteristics of individual cortical neuronal activity during mastication and the impact of tooth loss on these characteristics remain unclear. Thus, in this study, we aimed to determine the activity patterns of mastication-related motor cortical neurons elicited during mastication and examine the effects of tooth extraction on neuronal activity using two-photon Ca²⁺ imaging in head-restrained awake mice.</div></div><div><h3>Methods</h3><div>GCaMP6f-expressing adeno-associated virus serotype 1 was injected into the left motor cortex (centered 2 mm anterior and 2 mm lateral to the bregma) and electromyography (EMG) electrodes were implanted into the right masseter and digastric muscles of 6–8-week-old C57BL/6j mice. Three weeks after surgery, <em>in vivo</em> two-photon Ca²⁺ imaging of layer (L) 2/3 neurons and simultaneous EMG recordings were performed during the masticatory sequence.</div></div><div><h3>Results</h3><div>Mastication induced a remarkable increase in the power and frequency of Ca²⁺ responses and correlated with majority of the mastication-related motor cortical L2/3 neuronal activity. These mastication-related changes correlated with the activity of neurons with low baseline activity that occurred before mastication. Extraction of the right upper three molars caused clear neuroplastic changes in the mastication-induced Ca²⁺ activity of L2/3 neurons.</div></div><div><h3>Conclusions</h3><div>Our <em>in vivo</em> imaging study provides new insights into the neuronal basis of tooth loss-induced cortical neuroplasticity, and suggests a possible therapeutic approach for oral sensorimotor dysfunction.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100606"},"PeriodicalIF":2.6,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907728","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}

{"title":"Sex determination method using the third cervical vertebral body by head and neck CT","authors":"Akihiro Ochiai ,&nbsp;Atsushi Iwawaki ,&nbsp;Yusei Otaka ,&nbsp;Takeru Ishii ,&nbsp;Kota Ozawa ,&nbsp;Yuko Otomo ,&nbsp;Shinji Kito ,&nbsp;Hideki Saka","doi":"10.1016/j.job.2024.100608","DOIUrl":"10.1016/j.job.2024.100608","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to measure the volume of the third cervical vertebra using head and neck multi-detector computed tomography (MDCT) and establish a sex determination model based on sex differences in volume.</div></div><div><h3>Methods</h3><div>Head and neck CT images of 85 patients were obtained for dental diagnostic and therapeutic purposes. Digital Imaging and Communications in Medicine (DICOM) data obtained from head and neck CT were constructed using a three-dimensional image analysis software. A region of interest was created that included the entire third cervical vertebra and its volume was measured. Descriptive statistics were calculated for the measurements, and the means, standard deviations, and medians of the measurements were calculated separately for men and women. To create a sex determination model, binomial logistic regression analysis was performed using the training data group, with vertebral volume and sex as the explanatory and objective variables, respectively.</div></div><div><h3>Results</h3><div>The mean score of men was significantly higher than that of women. The sex determination model using the volume of the third cervical vertebral body resulted in an 80% correct sex classification rate.</div></div><div><h3>Conclusion</h3><div>The sex determination model can be used with other regional methods to aid sex determination.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100608"},"PeriodicalIF":2.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903708","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}

{"title":"Prrx2, the paired-related homeobox transcription factor, functions as a potential regulator of pannexin 3 expression in odontoblast differentiation","authors":"Manami Tanaka ,&nbsp;Asuna Sugimoto ,&nbsp;Kokoro Iwata ,&nbsp;Yumiko Nakashima ,&nbsp;Muhammad Dhiaulfikri Nauval Hadiana ,&nbsp;Yusuke Iwabuchi ,&nbsp;Kanae Wada ,&nbsp;Atsushi Oishi ,&nbsp;Tsutomu Iwamoto","doi":"10.1016/j.job.2024.100601","DOIUrl":"10.1016/j.job.2024.100601","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to elucidate the roles of Prrx1 and Prrx2, homeobox transcription factors, in tooth development and determine whether Prrx2 regulates pannexin 3 (Panx3) expression, which is important in preodontoblasts.</div></div><div><h3>Methods</h3><div>Tooth sections were prepared from 13.5-, 15.5-, and 18.5-day-old embryonic ICR mice, and Prrx1- and Prrx2-expressing cells were identified by <em>in situ</em> hybridization. To clarify the direct relationship between Prrx2 and Panx3, dual-luciferase reporter assay and electrophoretic mobility shift assay (EMSA) were performed. The effect of endogenous Prrx2 suppression on Panx3 expression was analyzed using an siRNA assay.</div></div><div><h3>Results</h3><div><em>In situ</em> hybridization revealed that in the molars, Prrx1 and Prrx2 were similarly expressed in the bud and cap stages; however, only Prrx2 was expressed in preodontoblasts at the bell stage. In the incisors, Prrx2-expressing cells were observed from dental papilla cells to preodontoblasts. In serial sections, Prrx2-expressing cells in preodontoblasts corresponded to Panx3-expressing cells. Luciferase reporter assay using luciferase reporter plasmids containing Panx3 promoter revealed that Prrx2 overexpression in HEK293 cells significantly increased luciferase activity. EMSA of nuclear extract proteins from Prrx2-overexpressing HEK293 cells or mouse dental papilla-derived cells to the Panx3 promoter showed the protein-probe complex bands. SiRNA assay revealed that Prrx2 knockdown inhibited Panx3 expression.</div></div><div><h3>Conclusions</h3><div>Our results suggest that Prrx2 may regulate Panx3 expression during odontoblastic differentiation.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100601"},"PeriodicalIF":2.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903692","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}

{"title":"Gene expression profiles in human dental pulp stem cells treated short-term with lipopolysaccharides before and after osteoinduction","authors":"Ai Orimoto ,&nbsp;Ziyi Wang ,&nbsp;Mitsuaki Ono ,&nbsp;Chiaki Kitamura ,&nbsp;Kentaro Ono","doi":"10.1016/j.job.2024.100603","DOIUrl":"10.1016/j.job.2024.100603","url":null,"abstract":"<div><h3>Objectives</h3><div>Dental pulp stem cells (DPSCs) are essential for reparative dentinogenesis following damage or infection. DPSCs surrounding theblood vessels in the central region of the dental pulp actively proliferate after tooth injury and differentiate into new odontoblast-like cells or odontoblasts to form reparative dentin. However, the signaling pathways involved in undifferentiated and osteodifferentiated DPSCs under inflammatory conditions remain unclear. This study aimed to compare the expression profiles of immortalized undifferentiated and osteo-differentiated human DPSCs (hDPSCs) treated with and without lipopolysaccharide (LPS) to elucidate the molecular regulatory mechanisms involved in inflammatory conditions.</div></div><div><h3>Methods</h3><div>We investigated the differences between undifferentiated and osteodifferentiated hDPSCs in response to LPS. RNA-seq analyses of undifferentiated and osteodifferentiated hDPSCs were performed with and without LPS.</div></div><div><h3>Results</h3><div>Whole-transcriptome profiling revealed distinct differences in the expression patterns of LPS-treated undifferentiated and osteodifferentiated DPSCs. Death-associated protein kinase 1 levels downregulated in LPS-treated osteodifferentiated cells, inhibiting apoptosis and enhancing cell survival After LPS treatment, osteodifferentiated DPSCs exhibited higher expression levels of various inflammatory cytokines and chemokines than undifferentiated DPSCs.</div></div><div><h3>Conclusion</h3><div>This study provides valuable transcriptomic data as a critical resource for uncovering potential therapeutic targets to enhance cell survival and regulate inflammation within the dental pulp. By elucidating the key molecular mechanisms and identifying specific gene expression changes linked to inflammatory and immune responses, these findings provide significant insights into osteo-differentiated hDPSCs.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100603"},"PeriodicalIF":2.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878193","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}

{"title":"The potential role of chromodomain helicase DNA-binding protein 3 in defining the cervical width by regulating the early growth stage of the apical papilla during tooth development","authors":"Kento Shimamura ,&nbsp;Toshiki Nojiri ,&nbsp;Hisatomo Kondo ,&nbsp;Yunosuke Ikeda ,&nbsp;Rika Yasuhara ,&nbsp;Hiroko Ida-Yonemochi ,&nbsp;Keishi Otsu ,&nbsp;Hidemitsu Harada ,&nbsp;Kenji Mishima ,&nbsp;Hayato Ohshima ,&nbsp;Takuya Kobayashi ,&nbsp;Tarou Irié","doi":"10.1016/j.job.2024.100604","DOIUrl":"10.1016/j.job.2024.100604","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to evaluate the role of the chromodomain helicase DNA-binding protein 3 (CHD3) in tooth morphogenesis in <em>Chd3</em> knockout mice.</div></div><div><h3>Methods</h3><div><em>Chd3</em> knockout mice were generated using the CRISPR-Cas9 method. Mandibular first molars were extracted from the mice and their littermates and morphometrically analyzed. Subsequent histological and immunohistochemical analyses of teeth were performed at each developmental stage. <em>Chd3</em> knockdown in mesenchymal cells from the dental papilla (mDP) and Hertwig's epithelial root sheath (HERS) was performed by <em>Chd3</em> shRNA transduction or a control using an adenoviral vector. These effects were examined using cell proliferation assays and quantitative real-time polymerase chain reaction.</div></div><div><h3>Results</h3><div>Narrowing of tooth cervical width was observed in mandibular first molars of <em>Chd3</em> knockout mice. On postnatal day (PN) 8, the cervical width was narrow before root formation in tooth germs. The number of Ki-67-positive cells decreased in the dental mesenchyme at PN1 and apical papilla at PN8. <em>Chd3</em> promoted the proliferation of dental mesenchymal cells, but no significant changes were observed in HERS epithelial cells. <em>Chd3</em> maintained sonic hedgehog (<em>Shh</em>) expression and inhibited that of bone morphogenetic protein (<em>Bmp</em>)<em>4</em> in dental mesenchymal cells, maintaining <em>Shh</em> and <em>Wnt3a</em> expression and inhibited that of <em>Bmp2</em> in HERS epithelial cells.</div></div><div><h3>Conclusion</h3><div><em>Chd3</em> may regulate tooth cervical width during the early growth stage of the apical papilla via <em>Shh</em>, <em>Bmp,</em> and <em>Wnt</em> signaling.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100604"},"PeriodicalIF":2.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878197","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}

{"title":"Low-molecular-weight polyphenol promotes cell sensitivity to cisplatin and alleviates cancer-related muscle atrophy via NF-κB suppression in oral squamous cell carcinoma","authors":"Yun-Ching Chang ,&nbsp;Yu-Yan Lan ,&nbsp;Hung-Yu Lin ,&nbsp;Cheng Liu ,&nbsp;Sue-Joan Chang","doi":"10.1016/j.job.2024.100595","DOIUrl":"10.1016/j.job.2024.100595","url":null,"abstract":"<div><h3>Objective</h3><div>Drug resistance and subsequent adverse effects, such as cancer cachexia, limit the clinical use of cisplatin. Oligonol® (Olg), a low-molecular-weight polyphenol, exhibits NF-κB inhibitory properties. NF-κB activation has been implicated in cisplatin resistance of cancer cells and skeletal muscle wasting. Therefore, we hypothesized that combined cisplatin and Olg could overcome chemoresistance and reduce muscle atrophy.</div></div><div><h3>Methods</h3><div>To investigate the efficiency of Olg, oral squamous cell carcinoma (OSCC) cells were used for chemosensitivity, and human skeletal muscle myoblast (HSkMC) was used for muscle atrophy. HSkMCs treated with OSCC cell-derived conditioned medium were used to examine the role of Olg in muscle atrophy mediated by the tumor inflammatory microenvironment.</div></div><div><h3>Results</h3><div>Olg exerted little effect on the viability of OSCC cells by promoting apoptotic cell death. However, it exhibited excellent capability to enhance the sensitivity of OSCC cells to cisplatin and overcome the acquired cisplatin resistance of OSCC. We revealed that NF-κB signaling contributes to cisplatin resistance in OSCC cells, whereas Olg enhances cell sensitivity to cisplatin by NF-κB suppression. Conversely, Olg contributes to a positive protein turnover and alleviates cisplatin-induced muscle atrophy by regulating Akt/mTOR/p70S6K and NF-κB/MuRF1 pathway. Olg represses TNF-α and interleukin 6 driven from OSCC cells and alleviates muscle atrophy mediated by the tumor inflammatory microenvironment.</div></div><div><h3>Conclusions</h3><div>Olg enhanced cisplatin chemosensitivity and reduced its adverse effects on skeletal muscle, suggesting its potential as a chemosensitizing agent for cisplatin. Further animal and clinical studies are required to validate these findings.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100595"},"PeriodicalIF":2.6,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873064","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}