Journal of Cellular Physiology最新文献

{"title":"Correction to “A Negative Feedback Loop of H19/miR-675/VDR Mediates Therapeutic Effect of Curcumin in the Treatment of Glioma”","authors":"","doi":"10.1002/jcp.70164","DOIUrl":"10.1002/jcp.70164","url":null,"abstract":"<p>Pan, J.-X., T.-N. Chen, K. Ma, S. Wang, C.-Y. Yang, and G.-Y. Cui. 2020. “A Negative Feedback Loop of H19/miR-675/VDR Mediates Therapeutic Effect of Curcumin in the Treatment of Glioma.” <i>Journal of Cellular Physiology</i>, 235, no. 3: 2171–2182.</p><p>1. Correction to authorship designation</p><p>In the originally published article, Mr. Tu-Nan Chen was indicated as a co–first author. Upon review, it has been determined that this designation does not accurately reflect the level of contribution. Mr. Tu-Nan Chen should be listed as the second author rather than as a co–first author.</p><p>The corrected author list is as follows:</p><p>Jie-Xiang Pan, Tu-Nan Chen, Kang Ma, Shi Wang, Chuan-Yan Yang, Gao-Yu Cui*</p><p>2. Correction to Figure 2</p><p>In Figure 2d and Figure 2h, the β-actin bands were inadvertently presented with overlapping image details. The corrected panels are provided above. The revised figures were generated from the original experimental data obtained from the same batch and time period.</p><p>This correction does not affect the results, statistical analyses, or the conclusions of the paper. All authors agree to the publication of this corrigendum.</p><p>The corrected Figure 2d and Figure 2h appear as above:</p><p>We apologize for this error.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70164","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147511985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PIEZO1 Channels Modulate the Small Extracellular Vesicle Release in C2C12 Cells","authors":"Bernareggi Annalisa,&nbsp;Zhang Wen Ru,&nbsp;Sanchez-Sanchez Laura,&nbsp;Norbedo Alessia,&nbsp;Fracassi Anna,&nbsp;Lucafò Marianna,&nbsp;Sciancalepore Marina,&nbsp;Alberto Griffoni,&nbsp;Russell K. William,&nbsp;Taglialatela Giulio,&nbsp;Lorenzon Paola,&nbsp;Limon Agenor","doi":"10.1002/jcp.70155","DOIUrl":"10.1002/jcp.70155","url":null,"abstract":"<p>PIEZO1 are mechanically-activated ion channels expressed in many cell types. Their pharmacological activation by the selective agonist Yoda1 has been reported to favor skeletal muscle regeneration by controlling the fate of myogenic precursors cells, but the underlying mechanisms remain largely unknown. Hereby, we investigated the possibility that PIEZO1 could control the release of small extracellular vesicles in myogenic C2C12 cells. Myoblasts and differentiated myotubes were treated with the PIEZO1 agonist Yoda1 (5 μM) for 24 hours. Released small extracellular vesicles were isolated by ultracentrifugation methods, and characterized by Western blotting, Nano Tracking and proteomic analysis. Pharmacological activation of PIEZO1 showed cell-type-specific effects: In myoblasts, Yoda1 treatment did not significantly affect the size or release of the small extracellular vesicles and resulted in only minor alterations to their proteomic profile. In myotubes Yoda1 treatment significantly increased small extracellular vesicles release and caused subtsantial alterations to the proteomic cargo. Notably, small extracellular vesicles released from both myoblasts and myotubes under PIEZO1 activation promoted myotube formation, though they did so through different capacities. Interestingly, in myotubes, Yoda1 also increased the expression of PIEZO1 protein of the vesicles suggesting a different biogenesis in undifferentiated and differentiated myogenic cells. Here, we propose PIEZO1 as a key element in controlling the release of small extracellular vesicles in myogenic precursors. Given the critical role of small extracellular vesicles in intercellular communication during muscle regeneration, our findings contribute to a better understanding of the role of PIEZO1 in the physiopathology of skeletal muscle tissue.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12989915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TMEM16A Contributes to Calcium-Activated Chloride Currents and Membrane Potential Changes in the Mouse Oocyte","authors":"Sarah Dalati,&nbsp;Vanessa J. Jones,&nbsp;Margot L. Day","doi":"10.1002/jcp.70159","DOIUrl":"10.1002/jcp.70159","url":null,"abstract":"<p>Oscillations in intracellular Ca²⁺ [Ca²⁺]_i are essential for mouse oocyte activation following fertilization. These [Ca²⁺]_i oscillations also induce repetitive hyperpolarizations in the membrane potential (Em). The present study aimed to identify the channels underlying the Em hyperpolarizations. Sulfhydryl reagents such as thimerosal, that oxidize the IP3-R channel, mimic the physiological changes at fertilization by eliciting simultaneous Em changes and [Ca²⁺]_i oscillations. Thimerosal-induced Em and [Ca²⁺]_i changes were prevented by the non-specific Ca²⁺-activated Cl^– channel (CaCC) inhibitors DIDS and NFA, as well as the TMEM16A/Anoctamin 1 CaCC specific inhibitor, T16Ainh-01. The K⁺ channel blocker TEA, and voltage-gated Cl^– channel blocker 9AC failed to inhibit the Em or [Ca²⁺]_i changes. TMEM16A protein was expressed in all stages of mouse preimplantation development, being localized at the plasma membrane in oocytes. Culture of zygotes in the TMEM16A inhibitor prevented development to the blastocyst stage. In summary, we present the first evidence for CaCC channels, namely TMEM16A, being critical for the initiation of Em hyperpolarisations in mouse oocytes.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12974648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct Thromboxane A₂–Dependent Pathways Regulate Arachidonic Acid–Triggered VASP Phosphorylation at Ser239 and Ser157 in Human Platelets: Real-Time Visualization Reveals Superior Antithrombotic Efficacy by Targeting Thromboxane A₂ Signaling over Cyclooxygenase Inhibition","authors":"Joen-Rong Sheu,&nbsp;Wei-Chieh Huang,&nbsp;Chao-Chien Chang,&nbsp;Chih-Wei Hsia,&nbsp;Chih-Hsuan Hsia,&nbsp;Thanasekaran Jayakumar,&nbsp;Shaw-Min Hou","doi":"10.1002/jcp.70160","DOIUrl":"10.1002/jcp.70160","url":null,"abstract":"<p>Platelets, as anucleate blood cells, play a pivotal role in the pathogenesis of cardiovascular diseases (CVDs), making antiplatelet therapy essential for preventing thrombotic events such as myocardial infarction. Thromboxane A₂ (TXA₂) is a key pro-aggregatory mediator that drives platelet activation. Phosphorylation of vasodilator-stimulated phosphoprotein (VASP) at Ser157 and Ser239 serves as a marker of cyclic nucleotide-mediated inhibitory signaling. The crosstalk between TXA₂ signaling and site-specific VASP phosphorylation in arachidonic acid (AA)-stimulated human platelets remains unclear and requires further investigation. In this study, AA at 60 µM induced maximal platelet activation, as evidenced by ultrastructural changes and increased P-selectin expression. Picotamide, a thromboxane synthase (TXS) inhibitor, effectively reversed AA-induced alterations, including ultrastructural remodeling, P-selectin expression, TXA₂ production, adenosine triphosphate (ATP)-release, mobilization of [Ca²⁺]ᵢ, and integrin α_IIbβ₃ activation. Importantly, picotamide's inhibition of platelet aggregation was unaffected by adenylate or guanylate cyclase inhibitors, suggesting a mechanism independent of cyclic nucleotide signaling. AA selectively increased VASP phosphorylation at Ser239, but not Ser157. While picotamide alone had no effect, its sequential administration with AA significantly enhanced Ser157 phosphorylation without altering Ser239 levels. These findings suggest that AA differentially regulates VASP phosphorylation sites via distinct mechanisms: Ser239 via a TXA₂-independent pathway associated with inhibitory signaling, and Ser157 via a TXA₂-dependent pathway linked to platelet activation. Finally, picotamide demonstrated superior antithrombotic efficacy compared to aspirin at an equivalent dose, as evidenced by real-time intravital imaging of thrombotic platelet plug formation in vivo. These results highlight TXS inhibition as a promising strategy for modulating platelet activation and thrombosis.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12969544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular pH and NHE1 Regulate Ductal Branching Morphogenesis in Organotypic Cultures of Human Pancreatic Duct Epithelial Cells","authors":"Daria Di Molfetta,&nbsp;Marilena Ardone,&nbsp;Francesca Fracasso,&nbsp;Maria Raffaella Greco,&nbsp;Grazia Tamma,&nbsp;Mariangela Centrone,&nbsp;Maria Barile,&nbsp;Maria Tolomeo,&nbsp;Alessia Nisco,&nbsp;Stephan Joel Reshkin,&nbsp;Rosa Angela Cardone","doi":"10.1002/jcp.70156","DOIUrl":"10.1002/jcp.70156","url":null,"abstract":"<p>Branching morphogenesis is a key process for constructing the tree-like architecture of multiple organs. The mechanisms regulating pancreatic ductal morphogenesis are still poorly understood, especially in the context of the particular pH dynamics of this organ. Indeed, ductal cells periodically release an alkaline juice to balance stomach acidity during digestion. This leads to a drop in extracellular pH (pHe) in the extracellular matrix (ECM) to maintain intracellular pH (pHi) homeostasis. Among the transporters involved in pH regulation, NHE1 also regulates epithelial branching morphogenesis in various tissues/organs. However, neither the effect of the changing pHe nor the role of NHE1 in branching morphogenesis has been investigated in a physiomimetic model in the human pancreas. Here, using 3D organotypic cultures of human pancreatic ductal cells (HPDE), we found that cells seeded on a Matrigel rich-ECM resembling normal ECM formed branched duct-like structures, which did not form on a more fibrotic Collagen I-rich ECM. Further, these cells overexpressed NHE1 mainly at the basolateral membrane. Ductal morphogenesis was affected by acidic pHe (pHe 6.7), which determined a hyper-branched network, and this was further increased by the inhibition of NHE1. We conclude that ECM composition and extracellular acidosis modulate branching morphogenesis in pancreatic ductal HPDE cells via NHE1 activity.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12954557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of Cellular Senescence by Pesticide Exposure in Human Umbilical Vein Endothelial Cells (HUVECs): Impacts on Telomerase Length, Cellular Morphology, and mtDNA Variation","authors":"Antonella Mazzone,&nbsp;Fani Konstantinidou,&nbsp;Daniela Lamanna,&nbsp;Ylenia Della Rocca,&nbsp;Valentina Gatta,&nbsp;Guya Diletta Marconi,&nbsp;Dainelys Guadarrama Bello,&nbsp;Rossana Falcone,&nbsp;Monica Mattioli-Belmonte,&nbsp;Antonio Nanci,&nbsp;Oriana Trubiani,&nbsp;Francesca Diomede,&nbsp;Jacopo Pizzicannella","doi":"10.1002/jcp.70150","DOIUrl":"10.1002/jcp.70150","url":null,"abstract":"<p>Chronic exposure to pesticides represents a substantial risk to human health; however, their role in promoting cellular senescence remains poorly understood. It's well known that endothelial dysfunction is an early hallmark of aging-related vascular damage. We employed Human Umbilical Vein Endothelial Cells (HUVECs) as an in vitro model for vascular endothelium to investigate whether pesticide exposure accelerates cellular senescence. The pesticides Boscalid (B), Pyraclostrobin (PY), Propamocarb (PR), and Lambda-cyhalothrin (LC) were tested individually and in combination. Following pesticide exposure, we evaluated cell viability through MTS assay, Endothelial Tube Formation by Scanning Electron Microscopy (SEM), alteration in mitochondria through Mitochondrial DNA Copy Number (mtDNA) variation, and TOM20 evaluation, Telomere Length reduction, expression of p21, reduced Ki67, and TERT through Immunofluorescence. Our findings suggest that pesticides accelerate senescence in endothelial cells.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 2","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12946610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147306349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMGB-1 Mediates The Exacerbation of Anaphylactic Shock Under Hyperlipidemic Conditions","authors":"Zikang Liu,&nbsp;Tingting Ding,&nbsp;Jing Wan,&nbsp;Zhihao Fan,&nbsp;Ziqi Yue,&nbsp;Kemiao Pang,&nbsp;Zhanfeng Jin,&nbsp;Weiwei Yang,&nbsp;Weihua Zhang,&nbsp;He Chen","doi":"10.1002/jcp.70154","DOIUrl":"10.1002/jcp.70154","url":null,"abstract":"<div>\u0000 \u0000 <p>Coronary heart disease (CHD) may worsen anaphylactic shock, but the exact mechanism is unknown. This study aimed to investigate the mechanisms by which coronary heart disease exacerbates anaphylaxis.C57BL/6 (WT) mice and LDLR^−/− mice were fed a high-fat diet for 20 weeks to develop atherosclerosis. Anaphylaxis was then induced using ovalbumin (OVA). Compared to WT mice, LDLR^−/− mice showed lower body temperature, worse pulmonary edema and higher mortality. Pulmonary endothelial cell CD31 (PECAM-1) expression decreased, but serum HMGB-1 levels increased. In vitro experiments found that ox-LDL exposure led to more HMGB-1 release from HUVECs. Moreover, ox-LDL induced mast cells release of histamine, upregulating the expression of more H1 receptors (H1R) in HUVECs, thereby further promoting HMGB-1 release. Pretreatment with an H1R inhibitor (chlorpheniramine) or an HMGB-1 neutralizing antibody improved survival and attenuated hypothermia in mice. In summary, ox-LDL exacerbates endothelial cell damage, resulting in increased HMGB-1 release and vascular permeability, which may worsen anaphylaxis to anaphylactic shock. The mechanisms are not fully understood, but HMGB-1 could be a potential target for future alleviation of anaphylactic shock.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 2","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acetyl-CoA Homeostasis via Mitochondrial Pyruvate Oxidation Governs Survival, Transcriptional Fidelity and Neural Specification in Primed Human Embryonic Stem Cells","authors":"Ning Zhong,&nbsp;Yujie Liu,&nbsp;Min Shao,&nbsp;Hanzhi Zhao,&nbsp;Yongqiang Wang,&nbsp;Junjie Gu,&nbsp;Qinwen Chen,&nbsp;Huiyong Yin,&nbsp;Ying Jin,&nbsp;Bing Liao","doi":"10.1002/jcp.70153","DOIUrl":"10.1002/jcp.70153","url":null,"abstract":"<div>\u0000 \u0000 <p>Human embryonic stem cells (hESCs) hold immense promises for regenerative medicine and exhibit two distinct pluripotency states: primed and naïve. However, metabolic regulation underlying these states remains incompletely understood. In particular, mitochondrial pyruvate oxidation in pluripotency regulation has not been documented. Here, we combined an inducible dihydrolipoamide S-acetyltransferase (<i>DLAT</i>) knockout model and pharmacological inhibition of mitochondrial pyruvate uptake (via the mitochondrial pyruvate carrier inhibitor UK5099) to dissect the state-specific effects of mitochondrial pyruvate oxidation in isogenic naïve and primed hESCs. Primed hESCs lacking <i>DLAT</i> or treated with UK5099 displayed pronounced cell death, reduced global protein acetylation levels, and transcriptional dysregulation. These defects were partially rescued by sodium acetate supplementation, implicating a reduction in acetyl-CoA abundance as a key mechanism. Notably, a set of neural lineage genes was specifically downregulated by disrupted mitochondrial pyruvate oxidation in primed hESCs, revealing the importance of mitochondrial pyruvate oxidation–mediated acetyl-CoA production in priming neural differentiation. In line with this, disruption of mitochondrial pyruvate oxidation impaired the differentiation process of primed hESCs towards neuroectoderm. In contrast, <i>DLAT</i> depletion in naïve hESCs did not affect cell growth and the naïve pluripotency state, highlighting the pluripotency state-dependent function of mitochondrial pyruvate oxidation. Our study uncovers the pivotal roles of mitochondrial pyruvate oxidation-mediated acetyl-CoA production for sustaining survival and transcriptional fidelity as well as facilitating neural differentiation in primed hESCs. Moreover, we emphasize that the function of mitochondrial pyruvate oxidation in hESCs is pluripotency state-dependent. These findings provide new cues for optimizing hESC maintenance and differentiation through targeted metabolic manipulation.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 2","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146219985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic Silencing of Primary Cilia Genes by PRAME and ETS2 in Melanoma Cells","authors":"Hyeon Ho Heo,&nbsp;HyeSook Youn,&nbsp;Eun-Yi Moon,&nbsp;Soo-Jong Um","doi":"10.1002/jcp.70151","DOIUrl":"10.1002/jcp.70151","url":null,"abstract":"<div>\u0000 \u0000 <p>Primary cilia are sensory organelles that regulate key signaling pathways essential for cell growth and differentiation. Loss of primary cilia is a common feature of melanoma and contributes to tumor progression, yet the underlying regulatory mechanisms remain poorly understood. In this study, we identify a transcriptional repression mechanism involving Preferentially Expressed Antigen in Melanoma (PRAME) and the transcription factor ETS2 as key modulators of ciliogenesis. We demonstrate an inverse correlation between PRAME expression and primary cilia formation in melanoma cells (R = −0.83, <i>p</i> = 0.042), and show that PRAME knockdown significantly promotes ciliogenesis, underscoring its role as a negative regulator. Integrative analyses combining our RNA-seq data with publicly available ChIP-seq data (GSE26439) and promoter motif analysis revealed that both PRAME and ETS2 are recruited to shared promoter regions of intraflagellar transport (IFT) genes, which are essential for cilia assembly. Notably, PRAME specifically interacts with ETS2, but not ETS1, indicating a selective and functionally relevant interaction. Similar to PRAME, ETS2 overexpression suppresses ciliogenesis and downregulates IFT gene expression. Mechanistically, the PRAME-ETS2 complex recruits histone deacetylase 1 (HDAC1) to IFT gene promoters, leading to epigenetic silencing via histone deacetylation. Together, these findings suggest that PRAME and ETS2 cooperatively suppress ciliogenesis in melanoma cells, proposing a previously unrecognized epigenetic mechanism of ciliary loss. This mechanism broadens our understanding of melanoma progression and highlights the role of the PRAME–ETS2–HDAC1 axis in regulating ciliogenesis.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 2","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146213184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Functions and Mechanisms of TGF-β3 Signalling in Controlling the Fate Determinations of Various Types of Stem Cells","authors":"Linzhi Kuang,&nbsp;Jianghong Xiang,&nbsp;Zuping He","doi":"10.1002/jcp.70152","DOIUrl":"10.1002/jcp.70152","url":null,"abstract":"<div>\u0000 \u0000 <p>The fate determinations of stem cells are governed by signalling molecules and pathways, and notably, the TGF-β superfamily members play pivotal roles in mediating these decisions. Significantly, TGF-β3 participates in affecting the development of stem cells and their microenvironment. In this review, we address the functions and regulatory networks of TGF-β3 in the fate decisions of several types of stem cells, including neural stem cells, haematopoietic stem cells, odontogenic stem cells, hair-follicle stem cells, adipose-derived stem cells, and mesenchymal stem cells. Specifically, we discuss the biosynthesis, activation, the roles, and mechanisms of TGF-β in influencing the proliferation, differentiation, and cell death of these stem cells, and we further highlight the perspective in this field. TGF-β signalling in stem cells begins with the activation of either integrin-dependent or integrin-independent pathways by binding to cell surface receptors TbRII and TbRI and co-receptor Betaglycan (TR3). TGF-β acts via both classical Smad signalling pathways and a variety of non-classical pathways. Notably, the biological functions of TGF-β3 depend primarily on specific cell type and the existing conditions of stem cells, reflecting the integration of multiple factors including the concentration, duration of action, interactions with other genes and/or non-coding RNAs. This review provides in-depth analyses of the molecular mechanisms through which TGF-β3 affects the fate decisions of adult stem cells, which lays a basis for identifying potential targets and developing future interventions for treating human diseases.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 2","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146213207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}