Frontiers in Cell and Developmental Biology最新文献

{"title":"Measles virus reprograms CD4⁺ T-cell sphingolipid and fatty acid metabolism to facilitate infection.","authors":"Maria Fernanda Grijalva Yépez, Yann Loïc Cordes, Agnes Fekete, Fabian Schumacher, Burkhard Kleuser, Elita Avota","doi":"10.3389/fcell.2026.1938931","DOIUrl":"10.3389/fcell.2026.1938931","url":null,"abstract":"<p><strong>Introduction: </strong>CD150-positive (CD150⁺) lymphocytes are the primary targets of measles virus (MV) infection during the acute phase. The depletion of infected CD150⁺ memory cells leads to a profound suppression of immune memory, resulting in increased susceptibility to secondary infections and severe complications in infected individuals. While lipids are known to be critical for viral life cycles, the specific lipid metabolic conditions facilitating MV replication in immune cells remain poorly understood.</p><p><strong>Methods and results: </strong>In this study, a comprehensive lipidomic analysis of MV-infected primary CD4⁺ T cells revealed significant alterations in three major lipid classes: sphingolipids, triacylglycerols, and glycerophospholipids. Specifically, MV infection increased the abundance of ceramides, dihydroceramides and triacylglycerols, while significantly reducing the levels of glucosylceramides and glycerophospholipids. Pharmacological intervention in the pathways of <i>de novo</i> sphingolipid synthesis, triacylglycerol synthesis and lipolysis significantly impaired measles virus replication in activated CD4⁺ CD150⁺ T cells.</p><p><strong>Discussion: </strong>Mechanistically, we demonstrate that MV glycoprotein-mediated membrane fusion, essential for viral entry and cell-to-cell spread, requires glucosylceramide synthase (GCS) activity and is further promoted by plasma membrane triacylglycerol content. Collectively, these findings highlight the essential role of MV-modulated triacylglycerol and sphingolipid metabolism in viral entry, dissemination, and intracellular replication within CD4⁺ T cells.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1938931"},"PeriodicalIF":5.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879287","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":"The substance P/ Neurokinin-1 receptor signaling drives perineural invasion in pancreatic ductal adenocarcinoma (PDAC).","authors":"Katja Schiedlauske, Sandra Biskup, Lina Hofer, Alina Deipenbrock, Kaan Çifcibaşı, Ihsan Ekin Demir, Irene Esposito, Dirk Weyhe, Nicole Elisabeth Teusch","doi":"10.3389/fcell.2026.1876023","DOIUrl":"10.3389/fcell.2026.1876023","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies, characterized by early metastasis, profound therapy resistance, and the highest prevalence of perineural invasion (PNI) among solid tumors. PNI fosters neuropathic pain and recurrence, ultimately correlating with poor survival. Sensory neurons promote PNI via neuropeptidergic signaling, including substance P (SP), while Schwann cells undergo injury-like reprogramming (GFAP&lt;sup&gt;+&lt;/sup&gt;/p75NTR&lt;sup&gt;high&lt;/sup&gt;), facilitating tumor invasion through chemoattractant secretion. Although the activation of neurokinin-1 receptor (NK-1R) via SP is implicated in tumor invasion and pain signaling, its role in coordinating bidirectional crosstalk within the PDAC neural niche remains elusive. In this study, we investigated the SP/NK-1R axis as a mediator of bidirectional crosstalk between tumor cells, sensory neurons, and Schwann cells in pancreatic cancer.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;To elucidate the role of the SP/NK-1R axis in perineural invasion, we employed a series of complementary &lt;i&gt;in vitro&lt;/i&gt; approaches. First, NK-1R expression was assessed by immunofluorescence in both primary PDAC tissue slices and PDAC tumor cell lines. To model the tumor-neural niche, MiaPaCa-2 cells were exposed to conditioned medium derived from iPSC-derived sensory neurons and primary human Schwann cells. Furthermore, to investigate the functional consequences of this signaling axis, we established a co-culture system composed of MiaPaCa-2 cells and Schwann cells, in which the number of invaded MiaPaCa-2 cells was quantified. Axon-guided tumor invasion was further examined using the OrganoPlate® Graft platform, where MiaPaCa-2 spheroids were co-cultured with sensory neurons. Moreover, NK-1R was pharmacologically inhibited using the FDA-approved antagonist aprepitant, and its effect on MiaPaCa-2 cell invasion was evaluated in both co-culture settings. Finally, the potential for therapeutic synergy was explored by combining aprepitant with the chemotherapeutic agent paclitaxel to assess potential synergy on cytotoxicity.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Immunofluorescence analysis of MiaPaCa-2, patient-derived tumor cells and primary PDAC tissue slices, revealed high NK-1R protein expression, establishing NK-1R as a putative clinically relevant target in PDAC. To model the bidirectional crosstalk within the PDAC niche, we examined NK-1R regulation under co-culture conditions. Conditioned media from sensory neurons and primary human Schwann cells significantly upregulated NK-1R expression in the MiaPaCa-2 cells. Reciprocally, exposure of both sensory neurons or Schwann cells to MiaPaCa-2 cells conditioned medium induced NK-1R upregulation, confirming bidirectional signaling. Consistent with this, supernatant from MiaPaCa-2/sensory neuron or MiaPaCa-2/Schwann cells co-cultures demonstrated a substantial increase in SP levels, indicating active neuropeptidergic communicat","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1876023"},"PeriodicalIF":5.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879549","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":"Programmed cell death-1: from a T-cell immune checkpoint to a regulator of Natural Killer cell biology.","authors":"Fabiana De Franco, Marco Greppi, Valentina Obino, Federico Rebaudi, Rayan Goda, Irene Caffa, Matteo Bozzo, Ombretta Melaiu, Enrico Munari, Valerio Gaetano Vellone, Camilla Jandus, Domenico Mavilio, Simona Candiani, Silvia Pesce, Emanuela Marcenaro","doi":"10.3389/fcell.2026.1924522","DOIUrl":"10.3389/fcell.2026.1924522","url":null,"abstract":"<p><p>Programmed cell death protein 1 (PD-1, CD279) is a pivotal inhibitory immune checkpoint receptor that plays a central role in maintaining immune homeostasis and peripheral tolerance. Originally characterized as a negative regulator of T-cell activation, PD-1 limits excessive immune responses and prevents autoimmunity, while its sustained expression under conditions of chronic antigen stimulation contributes to T-cell dysfunction and exhaustion. The discovery that blockade of the PD-1 pathway can restore anti-tumor immunity has revolutionized cancer therapy and established immune checkpoint inhibition as a cornerstone of modern oncology. Although PD-1 has traditionally been viewed as a key regulator of adaptive immunity, accumulating evidence indicates that its biological functions extend beyond T cells. In recent years, PD-1 expression has been identified in several innate immune cell populations, particularly Natural Killer (NK) cells, where it has emerged as an important modulator of effector functions, cytokine production, metabolic fitness, and antitumor activity. These findings have challenged the classical view of PD-1 biology and revealed unexpected similarities between NK-cell dysfunction and the exhausted phenotype described in chronically stimulated T cells. In the tumor microenvironment, PD-1 expression on NK cells has been associated with impaired cytotoxicity and reduced immune surveillance, suggesting that NK cells may also represent relevant targets of PD-1-mediated immunosuppression. At the same time, the mechanisms regulating PD-1 expression and signaling in NK cells appear to differ, at least in part, from those operating in T lymphocytes, highlighting the complexity of this pathway across distinct immune cell subsets. In this review, we summarize the current knowledge of PD-1 biology, from its established role in T-cell regulation to its emerging functions in NK cells. We discuss the molecular mechanisms governing PD-1 expression and signaling, its contribution to immune dysfunction in cancer and chronic diseases, and the potential implications of targeting the PD-1 axis to enhance both adaptive and innate antitumor immunity.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1924522"},"PeriodicalIF":5.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879363","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":"Craniofacial and dental toxicity of dioxins: developmental phenotypes and mechanistic insights.","authors":"Mohammadreza Vatankhah, Jian Xu","doi":"10.3389/fcell.2026.1878726","DOIUrl":"10.3389/fcell.2026.1878726","url":null,"abstract":"<p><strong>Background: </strong>Dioxins are persistent environmental pollutants with high lipophilicity and long half-lives, enabling their accumulation in biological tissues and ecosystems. Among them, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most toxic and extensively studied chemical. Human exposure occurs primarily through contaminated food, cigarette smoke, and industrial emissions, posing significant health risks.</p><p><strong>Objective: </strong>This review summarizes the effects of dioxins, particularly TCDD, on craniofacial and dental development and discusses recent findings on the mechanisms underlying these effects.</p><p><strong>Methods: </strong>A narrative review of experimental studies in animal models, <i>in vitro</i> systems, and human study data was conducted to evaluate phenotypic and mechanistic outcomes of TCDD exposure across palatogenesis, craniofacial bone formation, and tooth development.</p><p><strong>Results: </strong>In the developing palate, TCDD impairs mesenchymal proliferation, shelf elevation, and fusion, resulting in cleft palate involving various mechanisms such as oxidative stress, apoptosis, epigenetic changes, and suppression of TGF-β and Wnt signaling. Craniofacial bone development is also affected, with reduced ossification, altered mineralization, and impaired osteoblast differentiation. These outcomes are largely mediated by aberrant aryl hydrocarbon receptor (AhR) activation. However, other pathways, such as retinoic acid and vitamin D signaling, have also been found to have roles in these outcomes. Furthermore, genetic background modulates susceptibility, as shown by strain-specific differences and the protective role of AhR repressors. TCDD disrupts odontogenesis in a stage- and dose-dependent manner, leading to enamel hypoplasia, molar agenesis, dentin defects, and increased caries susceptibility.</p><p><strong>Conclusion: </strong>Dioxins, particularly TCDD, are potent developmental toxicants affecting multiple craniofacial tissues. Their effects are driven by dysregulation of several critical signaling pathways, with AhR acting as the central mediator. Given their long half-life and bioaccumulation, dioxins remain a relevant public health threat.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1878726"},"PeriodicalIF":5.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879796","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":"Synthesis of curcumin-derived carbon dots with dual antimicrobial and osteogenic properties for enhanced bone regeneration.","authors":"Yu Zhang, Lingyi Kong, Gang Dong, Qingqing Du","doi":"10.3389/fcell.2026.1865318","DOIUrl":"10.3389/fcell.2026.1865318","url":null,"abstract":"<p><strong>Introduction and aims: </strong>Infectious alveolar defects in dentistry present a persistent clinical dilemma, necessitating approaches that simultaneously promote osseous repair and suppress microbial adhesion. This study aimed to characterize the bifunctional properties of curcumin-derived carbon dots (Cur-CD) in facilitating the osteogenic commitment of rat bone marrow mesenchymal stem cells (rBMSCs) and exerting antibacterial effects, and offers foundational proof-of-concept data to support further evaluation in peri-implantitis-related infectious models.</p><p><strong>Methods: </strong>Cur-CD complex was synthesized and thoroughly characterized. Primary rBMSCs were isolated and cultured. The optimal working concentration of Cur-CD was identified via CCK-8 analysis. The cells were divided into control (Ctrl) and Cur-CD-treated groups. The degree of osteogenic differentiation was measured by Alizarin Red S staining, while protein and mRNA expression of key osteogenic markers (Runx2, OPN, Osterix, and OCN) were analyzed via Western blotting and quantitative real-time polymerase chain reaction, respectively. An oxidative stress model was established with H₂O₂, and cell migration was assessed by the transwell assay. The microbicidal properties against <i>Escherichia coli</i> and <i>Staphylococcus aureus</i> were examined using PI staining, plate colony counting, and inhibition zone assays.</p><p><strong>Results: </strong>The Cur-CD complex significantly enhanced mineralized nodule formation and upregulated both protein and mRNA expression of Runx2, OPN, Osterix, and OCN compared to the Ctrl group. Under H₂O₂-induced oxidative stress, Cur-CD treatment markedly promoted rBMSC migration. Additionally, the complex substantially increased bacterial mortality and reduced colony formation in <i>E. coli</i> and <i>S. aureus.</i></p><p><strong>Clinical relevance: </strong>These results demonstrate Cur-CD's dual osteogenic and antibacterial capacity, laying groundwork for future exploration of its utility against peri-implantitis-associated bone defects.</p><p><strong>Conclusion: </strong>The Cur-CD complex demonstrates promising dual functionality by enhancing osteogenic differentiation of rBMSCs and exerting robust antibacterial effects.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1865318"},"PeriodicalIF":5.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879490","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":"Tissue-specific oxidative stress and bleomycin hydrolase signatures are associated with organ-specific fibrotic responses in a mouse model of systemic sclerosis.","authors":"Rishabh Johri, Marianela Brizio, Maximilien Lora, Sydney Joy, James Martin, Inés Colmegna","doi":"10.3389/fcell.2026.1888823","DOIUrl":"10.3389/fcell.2026.1888823","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is a multisystem autoimmune disease characterized by inflammation, vasculopathy, and progressive fibrosis, yet the mechanisms underlying specific organ involvement are incompletely understood. Using the bleomycin-osmotic minipump (BLM-MP) mouse model, which recapitulates key clinical and histopathological features of SSc, we investigated whether tissue-specific oxidative stress responses and BLM metabolism are associated with divergent inflammatory and fibrotic remodeling across organs. Male C57BL/6 mice received continuous systemic infusion of BLM or saline for 7 days. Lungs, skin, kidneys, and liver were analyzed 14 and 28 days later by histopathology, collagen quantification, immunohistochemistry, and RT-qPCR. Systemic BLM exposure induced distinct organ-specific inflammatory, fibrotic and molecular responses. Progressive fibrosis and inflammatory infiltration developed predominantly in the lungs and skin, whereas the kidneys exhibited only mild focal cortical fibrosis and the liver remained largely unaffected. Fibrosis-prone organs displayed impaired antioxidant responses, characterized by reduced expression of superoxide dismutase 1 (<i>Sod1</i>), glutathione peroxidase 3 (<i>Gpx3</i>), and catalase (<i>Cat</i>), together with decreased expression of bleomycin hydrolase (<i>Blmh</i>), the enzyme responsible for BLM inactivation. In contrast, fibrosis-resistant organs exhibited preserved or increased expression of antioxidant enzymes and <i>Blmh</i> following BLM exposure, consistent with activation of protective redox and drug-clearance pathways. Across organs, lower antioxidant and <i>Blmh</i> expression was associated with greater inflammatory infiltration and collagen deposition. These findings identify a tissue-specific molecular signature with divergent inflammatory and fibrotic responses following systemic BLM exposure.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1888823"},"PeriodicalIF":5.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13529668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873594","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":"Emerging molecular mechanisms of the ECM-exosome growth-plate axis in idiopathic short stature.","authors":"Lizhen Piao, Hong Wang, Qiuying Zhang, Jinhe Li, Hongmei Sun, Ronghe Sun, Mingming Li, Ye Wang","doi":"10.3389/fcell.2026.1898879","DOIUrl":"10.3389/fcell.2026.1898879","url":null,"abstract":"<p><p>Idiopathic short stature (ISS) remains a clinically heterogeneous diagnosis in which impaired linear growth is often defined by exclusion rather than by mechanism. Increasing evidence suggests that ISS and related short-stature phenotypes may converge on overlapping growth-plate abnormalities characterised by disrupted chondrocyte proliferation, hypertrophic differentiation, extracellular matrix (ECM) maturation, mineralisation, and endochondral ossification. In this narrative review, we synthesize current evidence relevant to a proposed ECM-exosome growth-plate axis as a hypothesis-generating framework for ISS. The reviewed studies suggest that exosomal RNA dysregulation, ECM structural abnormalities, growth-hormone and insulin-like growth factor signalling variation, environmental and inflammatory exposures, and altered local signalling pathways may each contribute to impaired growth-plate output in specific experimental or clinical contexts. However, these diverse upstream routes appear to be associated with overlapping downstream abnormalities in chondrocyte state transition and cartilage-to-bone conversion. We propose that the cartilage ECM may function as a regulatory niche that could influence exosome diffusion, retention, uptake, spatial exposure, and RNA signalling activity within growth-plate chondrocytes. Conversely, exosomal miRNAs, lncRNAs, and circRNAs may regulate ECM synthesis, matrix remodelling, hypertrophy, and ossification. Accordingly, the axis is presented here as a hypothesis-generating model rather than as an established causal mechanism in ISS. Nevertheless, direct causal evidence remains limited, particularly regarding whether ECM composition, stiffness, proteoglycan density, collagen organisation, or mineralisation state governs exosome-mediated RNA delivery in human growth-plate models. Future studies should combine paediatric cohorts, human chondrocytes, growth-plate organoids, hPSC-derived cartilage systems, engineered exosomes, and ECM perturbation-rescue experiments to validate this axis. Defining ECM-exosome signatures may enable mechanism-based ISS subclassification, prediction of GH responsiveness, liquid-biopsy biomarker development, and growth-plate-targeted therapeutic strategies. Overall, the proposed ECM-exosome growth-plate axis may help frame ISS as a potentially molecularly stratifiable disorder involving chondrocyte state-transition failure, rather than solely as an endocrine diagnosis of exclusion.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1898879"},"PeriodicalIF":5.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13530325/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873622","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":"Exosomes as a biomarker in postoperative complications: a literature review.","authors":"Zhan Huang, Yi Wang, Wei Li, Zhiqiang Gan, Haiqing Yang, Jiayao Li, Yuan Jiang, Yi Yuan","doi":"10.3389/fcell.2026.1921951","DOIUrl":"10.3389/fcell.2026.1921951","url":null,"abstract":"<p><p>Surgery remains a common treatment, but it can lead to various potential complications. The incidence of complications after major surgery, in particular, is notably high. Postoperative complications contribute to increased patient morbidity and mortality. Timely and effective identification of these complications is essential for appropriate clinical management and improved patient outcomes. Exosomes are nano-sized membrane vesicles released by a variety of cell types, and play important roles in intercellular communications. Exosomal proteins and nucleic acids are involved in numerous physiological and pathological processes and are increasingly recognized as valuable biomarkers for disease diagnosis. Exosomes are present in all body fluids, which underlies their considerable potential as novel biomarkers in liquid biopsy. Previous research has reported that exosomes can serve as predictive biomarkers for several common postoperative complications, including neurocognitive disorders, allograft rejection, septic shock, atrial fibrillation, and sleep disturbance. These findings suggested that exosomes hold potential for application in the prevention and management of postoperative complications, representing an emerging direction in the investigation of postoperative biomarkers. Therefore, this review highlights the roles of exosomes in postoperative complications and discusses the challenges and opportunities of exosome-based diagnosis for these conditions.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1921951"},"PeriodicalIF":5.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13530329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873628","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":"Dynamic junction remodeling and transient vascular disruption during cancer cell extravasation across the blood-brain barrier.","authors":"Yu Zhang, Shunze Deng, Yonggang Ren, Jiulin Du, Bing Xu","doi":"10.3389/fcell.2026.1917794","DOIUrl":"10.3389/fcell.2026.1917794","url":null,"abstract":"<p><p>Brain metastasis is the major cause of cancer-related mortality and remains a critical challenge in clinical oncology. Extravasation of circulating cancer cells across blood-brain barrier (BBB) is the first crucial and rate-limiting step for brain metastasis growth. However, the dynamic changes of brain endothelial cell junction and vascular integrity during cancer cell extravasation across BBB remains unclear. Here, we established a knockin zebrafish line, <i>Ki(cdh5-eGFP)</i>, in which EGFP is fused to the C-terminal of endogenous VE-cadherin, enabling <i>in vivo</i> real-time imaging of brain endothelial junction dynamics. Then, we established a brain metastasis model in <i>Ki(cdh5-eGFP)</i> zebrafish, and tracked the multistep cascade of cancer cell extravasation across BBB. We demonstrated that cancer cells cross brain vascular endothelial cells, accompanied by dynamic remodeling of VE-cadherin and transient disruption of vascular integrity. Our model transforms the BBB into a dynamically observable interface, enabling real-time visualization of junction remodeling during cancer cell extravasation, which will not only facilitate further mechanistic study, but also provide a valuable platform for preclinical drug screening.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1917794"},"PeriodicalIF":5.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13529746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873555","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":"Telomerase expression and activity in the immortal cnidarian Hydra.","authors":"Dmitry A Skvortsov, Maria P Rubtsova, Vladimir S Dolzhnikov, Andrey G Zaraisky, Fedor M Eroshkin","doi":"10.3389/fcell.2026.1893030","DOIUrl":"10.3389/fcell.2026.1893030","url":null,"abstract":"<p><p>Hydra is one of the few known immortal animals, but the cellular and molecular mechanisms underlying this phenomenon remain largely unclear. Telomere lengthening is recognized as one of the factors contributing to enhanced proliferative potential at the cellular level. Telomerase activity is known to support both cellular and organismal longevity. In this study, we characterized the telomerase of <i>Hydra vulgaris</i>. The expression pattern of the telomerase catalytic subunit (<i>hyTERT</i>) mRNA correlates with regions exhibiting high proliferative potential and remains unchanged during budding or regeneration. These findings were further corroborated by measurements of telomerase activity. Our data suggest that telomerase may play a role in the immortality of <i>Hydra</i>.</p>","PeriodicalId":12448,"journal":{"name":"Frontiers in Cell and Developmental Biology","volume":"14 ","pages":"1893030"},"PeriodicalIF":5.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13529943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873568","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}