Journal of Oral Biosciences最新文献

{"title":"Apoptotic cell death during regressive changes in salivary glands: A morphological perspective","authors":"Shigeru Takahashi ,&nbsp;Akihiro Nezu ,&nbsp;Akihiko Tanimura ,&nbsp;Chikage Tamura ,&nbsp;Kenji Imamachi ,&nbsp;Tadasu Sato","doi":"10.1016/j.job.2024.100585","DOIUrl":"10.1016/j.job.2024.100585","url":null,"abstract":"<div><h3>Background</h3><div>Apoptosis was initially identified through transmission electron microscopy. Subsequent advances in morphological techniques for apoptosis detection have revealed its involvement in multiple pathological conditions in various tissues. This review summarizes previous experimental studies on apoptotic cell death during regressive changes in the salivary glands, with a focus on morphological observations.</div></div><div><h3>Highlight</h3><div>Obstructive sialadenitis is histologically characterized by acinar cell loss and increased number of duct cells. Although acinar cells were previously believed to dedifferentiate into duct cells, there is evidence that they are eliminated by apoptosis. Animals fed a soft diet exhibited parotid gland atrophy, in which acinar cells decreased in size and disappeared because of apoptosis. Age-related changes in the salivary glands involved a reduced number of acinar cell through apoptosis. Additionally, apoptotic acinar cell death occurs in other pathological conditions, including the regression of hypertrophic and irradiated salivary glands.</div></div><div><h3>Conclusion</h3><div>Apoptosis often eliminates acinar cells during atrophic alterations in the salivary glands. Unlike necrosis, apoptosis is an active form of cell death, thereby helping prevent the complete destruction of the salivary glands. However, the contribution of apoptosis to regressive changes in the salivary glands remains unclear and warrants further investigation.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100585"},"PeriodicalIF":2.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142569536","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":"Enhanced osteogenic differentiation of human periodontal ligament cells by mature osteoclasts","authors":"Sumit Suamphan ,&nbsp;Anupong Makeudom ,&nbsp;Suttichai Krisanaprakornkit ,&nbsp;Pimphorn Meekhantong ,&nbsp;Ekapong Dechtham ,&nbsp;Chidchanok Leethanakul","doi":"10.1016/j.job.2025.100632","DOIUrl":"10.1016/j.job.2025.100632","url":null,"abstract":"<div><h3>Objective</h3><div>Several <em>in vitro</em> studies have shown that reverse signaling from osteoclasts regulates osteoblast differentiation and mineralization. However, none of these studies have reported the effects of this signaling pathway on periodontal ligament (PDL) cells. Therefore, in this study, we aimed to investigate the interaction between receptor activators of nuclear factor kappa B (RANK) released from mature human osteoclasts and the membranous RANK ligand (RANKL) in human PDL cells.</div></div><div><h3>Methods</h3><div>Multinucleated mature human osteoclasts were differentiated from peripheral blood mononuclear cells upon incubation with recombinant macrophage colony-stimulating factor and RANKL. Mature osteoclasts and human PDL cells were characterized. A mature osteoclast-conditioned medium (OC-CM) was used to induce osteogenic differentiation of PDL cells. Mechanistic analysis of RANK-RANKL reverse signaling were conducted to determine the regulation of osteogenic induction using conditioned medium from mature osteoclasts treated with GW4869 (GW–OC–CM) or PDL cells pretreated with recombinant human osteoprotegerin (OPG).</div></div><div><h3>Results</h3><div>OC-CM significantly upregulated the mRNA expression of osteogenic genes and enhanced the osteogenic differentiation and biomineralization of PDL cells (<em>p</em> &lt; 0.05). GW–OC–CM significantly reduced the expression of osteogenic genes, osteogenic differentiation, and biomineralization in PDL cells (<em>p</em> &lt; 0.05). Similarly, the pretreatment of PDL cells with OPG before OC-CM treatment significantly reduced the osteogenic induction of PDL cells (<em>p</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Mature osteoclasts can induce osteogenesis in human PDL cells via RANK-RANKL reverse signaling.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 2","pages":"Article 100632"},"PeriodicalIF":2.6,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143478645","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":"TMPRSS2 expression in oral mucosal cells induced by transfected double-stranded RNA and IL-1β","authors":"Misaki Akagi ,&nbsp;Kouji Ohta ,&nbsp;Miyuki Sakuma ,&nbsp;Takako Naruse ,&nbsp;Yoko Ishida ,&nbsp;Chieko Niwata ,&nbsp;Nao Yamakado ,&nbsp;Takayuki Nakagawa ,&nbsp;Shigehiro Ono ,&nbsp;Hiromi Nishi ,&nbsp;Hideo Shigeishi ,&nbsp;Tomonao Aikawa","doi":"10.1016/j.job.2025.100619","DOIUrl":"10.1016/j.job.2025.100619","url":null,"abstract":"<div><h3>Objectives</h3><div>Transmembrane serine protease 2 (TMPRSS2) plays a key role in the entry of viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza A into host cells, and its elevated expression is a risk factor for the spread of viral infection. However, TMPRSS2 expression and the factors related to its induction in oral keratinocytes and fibroblasts remain largely unknown. Here, we examined TMPRSS2 expression and factors related to its induction in oral mucosal cells.</div></div><div><h3>Methods</h3><div>TMPRSS2 expression was examined in oral keratinocytes (RT7) and fibroblasts (GT1). Subsequently, TMPRSS2 induction in was analyzed in both cell types following transfection of nucleic acid and inflammatory cytokines, such as interleukin (IL)-1β. Finally, the effects of IL-1β on STAT1 activation related to double-stranded RNA (dsRNA)-induced TMPRSS2 expression were examined.</div></div><div><h3>Results</h3><div>RT7 and GT1 cells exhibited constitutive TMPRSS2 mRNA and protein expression. Transfection with Poly(I:C) (as a dsRNA) and poly (dA:dT) (as a double-stranded DNA [dsDNA]) increased TMPRSS2 expression. TMPRSS2 expression was also increased by IL-1β, but not IFN-γ or TNF-α, while the combination of IL-1β and transfected Poly(I:C) caused a dramatic increase in TMPRSS2 expression as compared to each alone in both cell types. IL-1β also enhanced transfected Poly(I:C)-activated STAT1 related to TMPRSS2 expression.</div></div><div><h3>Conclusions</h3><div>TMPRSS2-expressing oral keratinocytes and fibroblasts are targets of SARS-CoV-2 and influenza A virus. TMPRSS2 expression, in cooperation with IL-1β, plays an important role in promoting infection during virus invasion in oral mucosal cells.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 2","pages":"Article 100619"},"PeriodicalIF":2.6,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143450596","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":"Oral biosciences: The annual review 2024","authors":"Hayato Ohshima ,&nbsp;Kentaro Ono ,&nbsp;Kenji Mishima","doi":"10.1016/j.job.2025.100631","DOIUrl":"10.1016/j.job.2025.100631","url":null,"abstract":"<div><h3>Background</h3><div>The <em>Journal of Oral Biosciences</em> is committed to advancing and disseminating fundamental knowledge across all areas of oral biosciences. This editorial review features review articles covering diverse topics, including the “mandible,” “tooth remineralization,” “dental pulpitis,” “dental implants,” “mesenchymal stem cells,” “microbiota,” “facial pain,” “stomatitis,” “odontogenic tumors,” “oral submucous fibrosis,” “insights on orofacial pain,” “tissue engineering,” “melatonin,” and “regenerative medicine.”</div></div><div><h3>Highlight</h3><div>This editorial review focuses on forensic anthropology, calcium sucrose phosphate, pulp biomarkers, zirconia, mesenchymal stem cells, microflora, stomatitis, ameloblastoma, areca nut, orofacial pain, collagen, melatonin, and tooth regeneration.</div></div><div><h3>Conclusion</h3><div>The review articles featured in the <em>Journal of Oral Biosciences</em> have significantly contributed to expanding readers’ knowledge across various domains of oral biosciences. The current editorial review discusses the key findings and significance of these review articles.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100631"},"PeriodicalIF":2.6,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143442410","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":"MDP/NOD2 enhances RANKL-induced osteoclast differentiation of RAW264.7 cells","authors":"Wakana Sugimoto ,&nbsp;Hiroshi Inoue ,&nbsp;Nagako Sougawa ,&nbsp;Seiji Goda ,&nbsp;Aki Nishiura","doi":"10.1016/j.job.2025.100630","DOIUrl":"10.1016/j.job.2025.100630","url":null,"abstract":"<div><h3>Objective</h3><div>Receptor activator of nuclear factor-κB ligand (RANKL) is intimately involved in regulating bone remodeling during osteoclast differentiation and promotion of osteoclast function. Upon binding to its receptor, RANK, RANKL activates various signaling cascades that induce osteoclast differentiation of osteoclast precursor cells into osteoclasts. In the innate immune system, host pattern recognition receptors, such as Toll-like receptors and nucleotide-binding oligomerization domain-like receptors (NLRs), detect pathogen-associated molecular patterns and elicit an immune response. The NLR, nucleotide-binding oligomerization domain 2 (NOD2), is known to bind muramyl dipeptide (MDP) and regulate inflammatory responses via nuclear factor-κB (NF-κB). The objective of this study was to investigate the effect of MDP on RANKL stimulation of osteoclast differentiation to elucidate the mechanism of bone resorption in a bacterial infection-induced inflammation model.</div></div><div><h3>Methods</h3><div>The extent of osteoclast formation in MDP-stimulated RAW 264.7 cells was assessed using a tartrate-resistant acid phosphatase activity assay. The protein levels of intracellular signaling molecules were assessed by western blotting.</div></div><div><h3>Results</h3><div>In RAW 264.7 cells, MDP stimulation did not affect the expression of RANK. MDP enhanced the expression of osteoclast-specific proteins, such as nuclear factor of activated T cells 1 (NFATc1) and cathepsin K, which are osteoclast differentiation markers, in RANKL-stimulated RAW 267.4 cells. Furthermore, JSH23, an NF-κB inhibitor, suppressed the expression of NFATc1 after co-stimulation with MDP and RANKL.</div></div><div><h3>Conclusion</h3><div>MDP promoted osteoclast differentiation in RAW 267.4 cells by upregulating the activators, NF-κB and NFATc1, which are important for osteoclast differentiation, through enhancement of the RANKL signaling pathway.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100630"},"PeriodicalIF":2.6,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434151","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 genetic basis of micro-structural fragility in murine dentin: Insights from type 2 diabetes mellitus","authors":"Hideaki Inagawa ,&nbsp;Chie Watanabe ,&nbsp;Jun Zhou ,&nbsp;Yasutaka Sugamori ,&nbsp;Noriyuki Wakabayashi ,&nbsp;Kazuhiro Aoki ,&nbsp;Yo Shibata","doi":"10.1016/j.job.2025.100629","DOIUrl":"10.1016/j.job.2025.100629","url":null,"abstract":"<div><h3>Objectives</h3><div>Diabetes mellitus (DM) is a health issue affecting millions of people worldwide. Prolonged hyperglycemia increases the risk of pathological fractures; however, verifying this risk through bone analysis is challenging because of the heterogeneity of bone.</div></div><div><h3>Methods</h3><div>The systemic effects of type 2 DM (T2DM) on calcified tissues were investigated by examining dentin in mice, focusing on the underlying cellular and molecular mechanisms. Mouse incisor dentin was selected because of its continuous growth, similar to the annual rings of wood, offering a unique opportunity to study the time-dependent deterioration of calcified tissue affected by T2DM. RNA sequencing of pulp-derived cells was used to identify transcriptomic alterations in a db/db mouse model (BKS.cg-Lepr[db]/Lepr[<em>db</em>]Jc). Structural and mechanical changes in dentin were evaluated using Raman spectroscopy and nanoindentation.</div></div><div><h3>Results</h3><div>There was an increase in dentin volume in diabetic mice, accompanied by a deterioration in mechanical properties, particularly in primary dentin. This mechanical deterioration is likely to be associated with an inflammation-driven formation of abnormal dentin matrix caused by long-term hyperglycemia. No significant differences were observed in cross-linked collagen structures or advanced glycation end products.</div></div><div><h3>Conclusions</h3><div>The findings demonstrated that gene expression in T2DM affects dentin and bone, contributing to micro-structural fragility through protein production. The incisor model used in this study proved to be a versatile tool for assessing other diseases that affect the integrity of calcified tissues over time.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100629"},"PeriodicalIF":2.6,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143402029","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":"Dietary texture-driven masticatory activity and its impact on stress tolerance","authors":"Mie Kamate ,&nbsp;Hitoshi Teranishi ,&nbsp;Ryohei Umeda ,&nbsp;Kenshiro Shikano ,&nbsp;Shiho Kitaoka ,&nbsp;Toshikatsu Hanada ,&nbsp;Takatoshi Hikida ,&nbsp;Kenji Kawano ,&nbsp;Reiko Hanada","doi":"10.1016/j.job.2025.100628","DOIUrl":"10.1016/j.job.2025.100628","url":null,"abstract":"<div><h3>Objectives</h3><div>Although previous studies suggest that dietary texture-driven masticatory activity is correlated with stress tolerance, the underlying mechanisms, including neurotransmitter dynamics, remain unclear. This study investigated the effects of dietary texture-driven masticatory activity on stress tolerance in mice.</div></div><div><h3>Methods</h3><div>Behavioral responses to stress were assessed using the repeated social defeat stress (R-SDS) and social interaction test (SIT) model. Neurotransmitter levels in stress-related brain regions were analyzed in mice fed a solid diet (promoting masticatory activity) or a powdered diet (decreasing masticatory activity).</div></div><div><h3>Results</h3><div>Mice fed the powdered diet exhibited reduced stress tolerance compared with those fed the solid diet. Following the R-SDS, the powdered diet group displayed elevated gamma-aminobutyric acid (GABA) and norepinephrine levels in the prefrontal cortex. Before stress treatment, glutamic acid levels increased and those of choline decreased in the amygdala, whereas dopamine levels decreased in the powdered diet group after the R-SDS. In the locus coeruleus, mice on the powdered diet showed decreased glutamic acid and adenosine levels, alongside increased GABA levels. Serotonin levels decreased in the powdered diet group after the R-SDS, with no changes observed after the SIT. In the ventral hippocampus, GABA levels increased in the powdered diet group but decreased after the SIT.</div></div><div><h3>Conclusions</h3><div>This study demonstrates a correlation between masticatory activity and stress tolerance, evidenced by both behavioral and neurotransmitter changes. These findings suggest that reduced masticatory activity due to dietary texture contributes to decreased stress resilience.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100628"},"PeriodicalIF":2.6,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383549","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":"Signaling pathways of pro-IL-1β production induced by mechanical stress in gingival epithelial cells","authors":"Ruixuan Zhang ,&nbsp;Nagako Sougawa ,&nbsp;Dan Mao ,&nbsp;Hiroshi Inoue ,&nbsp;Seiji Goda","doi":"10.1016/j.job.2025.100626","DOIUrl":"10.1016/j.job.2025.100626","url":null,"abstract":"<div><h3>Objectives</h3><div>Mechanical stress on the teeth and alveolar bone caused by bruxism, orthodontics, and implants affects the periodontal tissues, causing gingival recession and alveolar bone resorption, and entire body, including the heart and vascular system. Although the same forces exerted on the alveolar bone and teeth are exerted on gingival epithelial cells, little is known about the effects of mechanical stress on these cells. This study investigated the effects of mechanical stress on gingival epithelial cells.</div></div><div><h3>Methods</h3><div>Ca9-22 cells (human gingival epithelial cells) were used. They were seeded onto the silicone and stretched cyclically. Mechanical stress-stimulated Ca9-22 cells were evaluated for pro-inflammatory interleukin (pro-IL)-1β production using Western blotting and analyzed to assess the phosphorylation level of intracellular signaling molecules.</div></div><div><h3>Results</h3><div>Mechanical stress induced pro-IL-1β upregulation in Ca9-22 cells, which was significantly inhibited by ruthenium red. Ruthenium red significantly inhibited mechanical stress-induced phosphorylation of focal adhesion kinase (FAK), P130cas, and extracellular signal-regulated kinase 1 and 2 (ERK1/2) induced by mechanical stress. Additionally, Y15 significantly inhibited the upregulation of pro-IL-1β expression and phosphorylation of FAK, P130cas, and ERK1/2 stimulated by mechanical stress.</div></div><div><h3>Conclusions</h3><div>In Ca9-22 cells, mechanical stress may increase pro-IL-1β production via mechanosensitive ion channels and FAK. These findings revealed the mechanisms of inflammation in mechanically-stressed Ca9-22 cells and may aid in the development of therapeutic approaches to prevent bone resorption.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100626"},"PeriodicalIF":2.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374568","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":"Zinc deficiency enhances salt preference through altered peripheral and central taste processing mechanisms","authors":"Akiyo Kawano ,&nbsp;Chizuko Inui-Yamamoto ,&nbsp;Yousuke Inoue ,&nbsp;Karen Yamauchi ,&nbsp;Namiki Kishigami ,&nbsp;Yusuke Yokota ,&nbsp;Susumu Tanaka ,&nbsp;Makoto Abe ,&nbsp;Takashi Maeda ,&nbsp;Shinsuke Ohba ,&nbsp;Hitoshi Niwa ,&nbsp;Satoshi Wakisaka","doi":"10.1016/j.job.2025.100627","DOIUrl":"10.1016/j.job.2025.100627","url":null,"abstract":"<div><h3>Objectives</h3><div>Zinc deficiency alters salt preference, however, the underlying mechanisms remain unclear. We hypothesized that altered salt preference, during zinc deficiency, is associated with brainstem and hypothalamic nuclei modified activity which is involved in the gustatory processing and fluid balance regulation.</div></div><div><h3>Methods</h3><div>This study elucidated the abnormal intake of high-concentrated sodium chloride solution caused by zinc deficiency in taste reception, taste nerve, and brain. Initially, we performed taste behavioral tests including the chorda tympani (CT) nerve transection (CTx) and the sodium channel blocker. Secondly, the neural activity in the aforementioned regions was investigated by assessing the c-Fos-like protein expression, as a marker of neuronal activity, in the parabrachial nuclei (PBN) for the taste pathway, as well as in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) for fluid regulation-related areas.</div></div><div><h3>Results</h3><div>Zinc-deficient Sprague-Dawley rats showed increased licking responses and preference for high salt concentrations compared to the controls. Neither the CTx nor the administration of amiloride, a sodium channel blocker, affected NaCl preference in zinc-deficient rats. High salt stimulation induced significantly fewer c-Fos-immunoreactive neurons in the PBN, SON, and PVN of zinc-deficient rats compared to controls.</div></div><div><h3>Conclusions</h3><div>These findings suggest that zinc deficiency disrupts NaCl reception and alters neuronal responses to NaCl in the gustatory pathway and fluid balance regulation, potentially leading to modified NaCl ingestive behaviors. Our results provide new insights into the neural mechanisms underlying taste dysfunction and altered salt preference in zinc deficiency.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100627"},"PeriodicalIF":2.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374694","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":"Effect of short-term gravitational changes on the human minor salivary gland stem cell characteristics","authors":"Jeong Mi Kim ,&nbsp;Tri Ho Minh ,&nbsp;Eun Jeong Jeon ,&nbsp;Jin Mi Park ,&nbsp;Sungryeal Kim ,&nbsp;Jeong-Seok Choi","doi":"10.1016/j.job.2025.100625","DOIUrl":"10.1016/j.job.2025.100625","url":null,"abstract":"<div><h3>Objectives</h3><div>Human minor salivary gland stem cells (huMSGSCs) are promising in regenerative medicine. Their multipotent capabilities enable tissue regeneration and offer treatment potential for various diseases. The effects of hypergravity (HyperG) and microgravity (MicroG) on stemness and therapeutic potential are not well explored. Therefore, this study investigated the effects of short-term HyperG and MicroG exposure on huMSGSC stemness and differentiation potential for treating salivary gland dysfunction.</div><div>Methods: huMSGSCs were exposed to 1G, MicroG, and HyperG. Cell morphology, proliferation, sphere formation, and differentiation potential were analyzed. Stem cell and tight junction markers were evaluated using flow cytometry, real-time PCR, Western blot, and immunofluorescence analysis.</div></div><div><h3>Results</h3><div>huMSGSCs showed fibroblast-like morphology and robust proliferation up to passage 10. Differentiation into adipocytes, chondrocytes, and osteocytes was successful, despite enhanced lineage-specific marker expression. HyperG significantly increased proliferation at 48 and 72 h, MicroG-exposed cells formed more numerous and smaller spheres, and HyperG-exposed cells produced larger spheres. HyperG elevated stem cell marker (CD90, LGR5, SOX2) expression levels, and the expression of tight junction protein expressions (ZO-1, ZO-2) was higher under HyperG treatment.</div></div><div><h3>Conclusions</h3><div>Short-term HyperG and MicroG exposure differentially influenced huMSGSC stemness and differentiation potential. HyperG enhanced proliferation, stem cell marker expression, and differentiation capacity. These findings suggest the potential of optimizing huMSGSCs for regenerative therapies that target salivary gland dysfunction and other tissue regeneration applications.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100625"},"PeriodicalIF":2.6,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366201","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}