Biology of the Cell最新文献

{"title":"Functional and Morphological Plasticity of the Endolysosomal System: Pigment Organelles at the Crossroads of Physiology and Pathology","authors":"Laura Salavessa,&nbsp;Myckaëla Rouabah,&nbsp;Paula Pernea,&nbsp;Smail Hadj-Rabia,&nbsp;Cédric Delevoye","doi":"10.1111/boc.70036","DOIUrl":"10.1111/boc.70036","url":null,"abstract":"<p>The endolysosomal system is a highly dynamic and versatile network of organelles essential for maintaining cellular and tissue homeostasis. Its functional diversity relies on a high degree of plasticity, driven by tightly regulated membrane remodeling and intracellular trafficking events. In certain specialized cells, this plasticity enables the formation of lysosome-related organelles, like melanosomes in pigment cells, through the repurposing of ubiquitous membrane trafficking machineries. Disruption of these pathways can lead to pathological conditions, including genetic disorders. In this review, we explore how endolysosomal plasticity underlies key adaptive cellular strategies at the cellular and tissue levels. Focusing on melanocytes, which synthesize melanin, and keratinocytes, which receive and store it, we illustrate how trafficking and membrane dynamics events coordinate between these two cell types for skin pigmentation and photoprotection, and how mutations affecting these processes lead to genetic forms of albinism. By using skin pigmentation as a model of cell- and tissue-specific adaptation, this review highlights the broader physiological and pathological implications of endolysosomal membrane morphodynamics.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 10","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.70036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How Human Induced Pluripotent Stem Cells-Derived Models can Advance our Understanding of Secretion Mechanisms in Physiological and Pathological Contexts?","authors":"Lou Fourriere,&nbsp;Gaelle Boncompain","doi":"10.1111/boc.70035","DOIUrl":"10.1111/boc.70035","url":null,"abstract":"<div>\u0000 \u0000 <p>The molecular architecture of differentiated cells is essential to ensure their specific functions and is supported by membrane trafficking. Defects in the intracellular organization and/or in protein transport contribute to various diseases such as neurological and cardiac diseases. In the recent years, human induced pluripotent stem cells (hiPSCs) have been used to model diseases. Indeed, pluripotent stem cells represent a powerful model to reveal differences in the organization and functional capacity of the secretory trafficking routes responsible for the complex morphology and specialized functions of differentiated cells. This review focuses on the need to conduct investigations of the membrane trafficking mechanisms, their regulation and defects in hiPSCs-derived models, such as neurons and cardiomyocytes, and highlights how powerful these models are to unravel cell-type specific properties. Some studies conducted in hiPSCs-derived models deciphering trafficking defects in pathological conditions are cited as examples. New advances in genome editing, intracellular tools, high-resolution microscopy and fast imaging are essential for studying membrane trafficking in hiPSCs, which will be discussed, as well as their current limitations and areas of improvement. Altogether, this review is intended to pave the way for interconnected comparative studies required to understand the mechanisms regulating protein transport in health and disease.</p>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 10","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Membrane Bound E-Cadherin Stimulates PI3K/Akt Signaling","authors":"Aurora Candelario-Martínez,&nbsp;Mónica Vizcarra-Soto,&nbsp;Nicolás Villegas-Sepúlveda,&nbsp;Porfirio Nava","doi":"10.1111/boc.70034","DOIUrl":"10.1111/boc.70034","url":null,"abstract":"<p>Cell junction proteins play a pivotal role in regulating key physiological processes, including proliferation and apoptosis. E-cadherin, a crucial component of adherens junctions, is essential for maintaining intestinal epithelial homeostasis by modulating cell adhesion and proliferation. In this study, we explored the function of E-cadherin in the intestinal epithelial cells. Our findings indicate that during colitis, E-cadherin remains associated with the cell membrane in colonocytes. Furthermore, using an in vitro system, we demonstrated that in colonocytes, E-cadherin inhibits cell proliferation and β-catenin signaling while simultaneously activating the PI3K/Akt pathway. These results suggest that E-cadherin may suppress cell proliferation while promoting PI3K/Akt signaling in colonocytes of colitic mice.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 10","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.70034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recombinant Human Fibronectin Mediates Macrophage Polarization via NF-κB/TGF-β1 Pathway to Enhance Fibroblast Proliferation","authors":"Zongbao Zuo,&nbsp;Zizheng Yang,&nbsp;Jun Zhao,&nbsp;Lei Han,&nbsp;Jing Yang,&nbsp;Yueping Wang,&nbsp;Ziyun Zhang,&nbsp;Daoping Zhou","doi":"10.1111/boc.70025","DOIUrl":"10.1111/boc.70025","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This research aims to explore the molecular mechanism where recombinant human fibronectin (rhFN) regulates macrophage polarization and then affects fibroblast proliferation via the nuclear factor kappa B (NF-κB)/transforming growth factor β1 (TGF-β1) signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Macrophages RAW 264.7 were activated with LPS and subsequently treated with rhFN, followed by flow cytometry to assess macrophag polarization. Cytokine levels of interleukin (IL)-10 tumor necrosis factor alpha (TNF-α), IL-6, and Arg-1, as well as TGF-β1, were measured using enzyme-linked immunosorbent assay (ELISA). Fibroblast NIH 3T3 was cultured with macrophage-conditioned media (CM), and CCK-8, cell adhesion, and wound healing assays were used to evaluate their proliferation, adhesion, and migration capacities. Western blot was conducted to detect the changes of proteins related to TGF-β1/Smad2/3 and NF-κB signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>RhFN significantly promoted macrophage M2 polarization and increased TGF-β1 secretion while reducing pro-inflammatory cytokines TNF-α and IL-6, increasing IL-10 and Arg-1 levels. Fibroblasts cultured with rhFN-treated macrophage-CM showed increased Smad2/3 phosphorylation, causing improved proliferation, adhesion, and migration abilities. Inhibition of NF-κB signaling promoted an anti-inflammatory macrophage profile, while NF-κB activation partially reversed rhFN's effects on fibroblast function. Inhibition of TGF-β1 resulted in reduced fibroblast proliferation, adhesion, and migration abilities, confirming its pivotal role in rhFN-mediated effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>RhFN modulates macrophage polarization through NF-κB inhibition and promotes fibroblast proliferation, adhesion, and migration via TGF-β1/Smad2/3 signaling.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 9","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DeepSCEM: A User-Friendly Solution for Deep Learning-Based Image Segmentation in Cellular Electron Microscopy","authors":"Cyril Meyer,&nbsp;Victor Hanss,&nbsp;Etienne Baudrier,&nbsp;Benoît Naegel,&nbsp;Patrick Schultz","doi":"10.1111/boc.70032","DOIUrl":"https://doi.org/10.1111/boc.70032","url":null,"abstract":"<p>Deep learning methods using convolutional neural networks are very effective for automatic image segmentation tasks with no exception for cellular electron micrographs. However, the lack of dedicated easy-to-use tools largely reduces the widespread use of these techniques. Here we present DeepSCEM, a straightforward tool for fast and efficient segmentation of cellular electron microscopy images using deep learning with a special focus on efficient and user-friendly generation and training of models for organelle segmentation.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 9","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.70032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144923336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 Synchrony of STARD4-AS1 and H19 Downregulation with Cardiomyocytes Cell Cycle Arrest","authors":"Mahshad Shiri,&nbsp;Fatemeh Movahedi,&nbsp;Fatemeh Etezadi,&nbsp;Iman Bhia,&nbsp;Eberhard Korsching,&nbsp;Kai Wang,&nbsp;Sedigheh Gharbi,&nbsp;Sara Pahlavan","doi":"10.1111/boc.70028","DOIUrl":"https://doi.org/10.1111/boc.70028","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiac regeneration is hindered by the permanent cell cycle arrest of cardiomyocytes post-birth, leading to compensatory fibrosis and impaired cardiac function after injury. While the role of cell cycle regulatory proteins is well understood, the impact of long non-coding RNAs (lncRNAs) remains unclear. To address this gap, we reanalyzed public transcriptomic datasets comparing pre- and post-natal ventricular cardiomyocytes. In silico analysis identified differentially expressed lncRNAs, with four candidates selected for further validation. Human embryonic stem cells (hESCs) were differentiated into cardiomyocytes, and their cell cycle status was assessed on Days 10, 20, and 30. The expression of in silico-identified lncRNAs was evaluated in proliferative (Day 10) and non-proliferative (Days 20 and 30) hESC-derived cardiomyocytes, resembling pre- and post-natal ventricular cardiomyocytes. Among the candidates, STARD4-AS1 and H19 showed a permanent downregulation pattern in both in silico and in vitro assays. STARD4-AS1 and H19 lncRNAs might reside in the regulatory network of cardiomyocytes cell cycle arrest and as targets for cardiac regenerative strategies.</p>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 8","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SOX15 Transcriptionally Decreases the Level of MMP2 and Inhibits Vasculogenic Mimicry to Slow Down the Progression of Ovarian Cancer","authors":"Xiaodan Zhao,&nbsp;Xinjia Wang,&nbsp;Chao Wang,&nbsp;Huiyu Tian,&nbsp;Yang Zhou,&nbsp;Lihong Gong","doi":"10.1111/boc.70031","DOIUrl":"https://doi.org/10.1111/boc.70031","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>Vascular mimicry (VM) is pivotal for promoting tumor cell proliferation and invasion in ovarian (OV) cancer patients. Sex-determining region Y-box 15 (SOX15) suppresses the malignant growth of tumor cells. However, the function of SOX15 in OV cancer remains undefined. Using SKOV-3 and ES2 cell lines, along with xenograft models in nude mice, we investigated the effects of SOX15 on tumor cell growth and VM formation in OV cancer, as well as the underlying mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We found that SOX15 inhibited the proliferation, migration, and invasion of SKOV-3 cells. SOX15 overexpression reduced VM formation in SKOV-3 cells, accompanied by decreased levels of VE-cadherin and vascular endothelial growth factor A (VEGFA). Similarly, SOX15 suppressed ES2 cell proliferation and motility. Additionally, xenograft experiments demonstrated that SOX15 knockdown increased tumor volume in mice, along with upregulated expression of Ki67 and matrix metalloproteinase-2 (MMP2) in tumor tissues. CD31/PAS double staining revealed that silencing SOX15 promoted VM formation in tumors. Mechanistically, SOX15 overexpression downregulated MMP2 at both mRNA and protein levels, suppressing VM formation and thereby slowing OV cancer progression. Dual-luciferase reporter assays revealed that SOX15 overexpression inhibited MMP2 promoter activity, and chromatin immunoprecipitation followed by PCR (ChIP-PCR) confirmed the direct binding of SOX15 to the MMP2 promoter.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our results indicate that SOX15 transcriptionally represses MMP2 expression, thereby inhibiting VM formation and ultimately suppressing OV cancer initiation and progression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>We establish a theoretical foundation for developing novel therapeutic approaches targeting the SOX15/MMP2 axis in OV cancer treatment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 8","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144869702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PU.1 Facilitates Endothelial-to-Mesenchymal Transition in Cardiac Endothelial Cells","authors":"Ran Meng,&nbsp;Bin Huang,&nbsp;Fan Yang,&nbsp;Nannan Zhang,&nbsp;Bin Feng,&nbsp;Dalong Zhu","doi":"10.1111/boc.70029","DOIUrl":"https://doi.org/10.1111/boc.70029","url":null,"abstract":"<div>\u0000 \u0000 <p><b>Background</b>: The endothelial-to-mesenchymal transition (EndMT) plays a critical role in cardiac fibrosis pathogenesis. However, the molecular mechanisms driving EndMT remain poorly understood. This study investigates the regulatory function of the transcription factor PU.1 in EndMT using primary cardiac endothelial cells.</p>\u0000 <p><b>Methods</b>: Immunofluorescence was performed to assess characteristic protein markers in cultured cells. PU.1 knockdown was achieved through siRNA transfection. Key gene expression was quantified at mRNA and protein levels. EndMT progression was evaluated via migration and tube formation assays. Additionally, immunoprecipitation was utilized to examine PU.1 interaction with phosphorylated Smad3 (p-Smad3).</p>\u0000 <p><b>Results</b>: TGF-β1-induced EndMT is coupled with a significant upregulation of PU.1 expression. PU.1 silencing attenuated EndMT, evidenced by elevated CD31/VE-cadherin and reduced α-SMA/N-cadherin/FSP-1 levels under TGF-β1 stimulation. PU.1 knockdown functionally impaired cell migration while promoting vascular lumenogenesis. Conversely, forced PU.1 expression was sufficient to drive EndMT in cardiac endothelial cells. Mechanistically, our data suggest that PU.1 enhances Smad3 phosphorylation, potentially through direct binding to and stabilization of the p-Smad3 protein.</p>\u0000 <p><b>Conclusion</b>: PU.1 drives EndMT in cardiac endothelial cells by enhancing Smad3 phosphorylation and stability. These results elucidate novel molecular pathways in EndMT and identify PU.1 as a potential therapeutic target for attenuating cardiac fibrosis.</p>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144716735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Chronological Trigger: The Orchestra Between Homeobox Genes and the Circadian Clock During Development","authors":"Joice de Faria Poloni,&nbsp;Bruno César Feltes","doi":"10.1111/boc.70027","DOIUrl":"https://doi.org/10.1111/boc.70027","url":null,"abstract":"<p>As master regulators of embryonic development, regulating homeobox genes is fundamental for developmental biology. Despite the growth of multiple topics regarding fine-tuning homeobox gene expression, the discussion on how the circadian rhythm affects their control and vice-versa still needs to be improved. Due to the intrinsic importance of the circadian clock and its impact on several molecular mechanisms, including development and pregnancy, the interplay between this mechanism and homeobox genes becomes a meaningful discussion. This work aims to review and critically discuss the crosstalk between homeobox genes and circadian regulation in multiple organisms, focusing on differentiation and developmental mechanisms. A considerable focus is given to new perspectives on the topic.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.70027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144695794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Meeting Report on the Symposium Organized to Celebrate the 40th Anniversary of the French Society for Cell Biology","authors":"Florence Niedergang,&nbsp;Renaud Chabrier,&nbsp;Isabelle Tardieux","doi":"10.1111/boc.70014","DOIUrl":"https://doi.org/10.1111/boc.70014","url":null,"abstract":"<p>The French Society for Cell Biology (SBCF) gathers all researchers working in the broad field of cell biology and is actively involved in several missions. Indeed, from communicating about the latest breakthroughs to announcing upcoming events, the SBCF also identifies and nurtures emerging talents while financially supporting young researchers to help them attend scientific meetings. The society's mission is to promote the scientific area, to boost knowledge transmission, and be the reference for French research in cell biology on the international stage. In this context, the SBCF has woven networks of knowledge and expertise with global Societies of cell biology and continues to foster partnerships specifically through joint sessions at international meetings. In the same vein, since 2022, the SBCF has been organizing an annual themed international symposium called “Cell Biology of…” to spotlight specific topics of interest. Past editions have highlighted subjects such as the coronaviruses, neurons, and plants, showcasing the broad scope of the discipline. In addition to these scientific initiatives, the SBCF is also very much committed to supporting and regularly organizing a variety of events for raising the public awareness of science in general and cell biology in particular, and engaging it in the wonders of science.</p>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":"117 7","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.70014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144635339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}