European journal of cell biology最新文献

{"title":"The role of prostanoids in regulatory T cells and their implications in inflammatory diseases and cancers","authors":"Somsak Prasongtanakij ,&nbsp;Kitipong Soontrapa ,&nbsp;Dean Thumkeo","doi":"10.1016/j.ejcb.2025.151482","DOIUrl":"10.1016/j.ejcb.2025.151482","url":null,"abstract":"<div><div>Regulatory T cells (Tregs) play an important role in the immune system through the regulation of immunological self-tolerance and homeostasis. Furthermore, increasing evidence suggests the potential contribution of Tregs beyond immunity in the process of repairing various injured tissues. Tregs are generally characterised by the constitutive expression of forkhead box protein 3 (FOXP3) transcription factor in the nucleus and high expression levels of CD25 and CTLA-4 on the cell surface. To date, a large number of molecules have been identified as key regulators of Treg differentiation and function. Among these molecules are prostanoids, which are multifaceted lipid mediators. Prostanoids are produced from arachidonic acid through the catalytic activity of the enzyme cyclooxygenase and exert their functions through the 9 cognate receptors, DP1‐2, EP1-EP4, FP, IP and TP. We briefly review previous studies on the regulatory mechanism of Tregs and then discuss recent works on the modulatory role of prostanoids.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151482"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143767452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transient pharmacological inhibition of SUMOylation during pregnancy induces craniofacial malformations in offspring mice","authors":"Jorge Mata-Garrido ,&nbsp;Isabella Zafferri ,&nbsp;Alice Nordlinger ,&nbsp;Yann Loe-Mie ,&nbsp;Anne Dejean ,&nbsp;Jack-Christophe Cossec","doi":"10.1016/j.ejcb.2025.151480","DOIUrl":"10.1016/j.ejcb.2025.151480","url":null,"abstract":"<div><div>Cell identity plays a pivotal role in embryo development, guiding the process of cellular differentiation essential for tissue and organ formation. Post-translational modification by the ubiquitin-related SUMO protein acts as a chromatin barrier to cell fate conversions. While SUMOylation deficiency is incompatible with mammalian embryonic development, haploinsufficiency for the SUMOylation machinery's E1 enzyme, UBA2, leads to various phenotypic traits in humans, including craniofacial malformations and aplasia cutis congenita. To investigate SUMO's role in organogenesis, SUMOylation was transiently suppressed using a specific pharmacological inhibitor, TAK981, administered during the early post-implantation embryo stage. A high-concentration injection led to embryonic lethality associated with epigenetic scars and alterations in nuclear and nucleolar integrity observed in treated embryo-derived fibroblasts. Lower-concentration injections resulted in viable mice with craniofacial deformities often accompanied by hydrocephalus, syndactyly and an aplasia cutis-like phenotype. Transcriptomic analysis revealed the repression of genes involved in neural crest differentiation in the TAK981-treated embryos as well as the overexpression of the <em>Fgfr</em> gene family in the adult TAK981 progeny. These genes, expressed in neural crest derivatives, are known for their gain-of-function mutations linked to human craniosynostosis syndromes, suggesting that potential overactivation of the FGF signaling pathway may contribute to the malformations observed in TAK981 progeny. Altogether, disruption of the SUMOylation/deSUMOylation equilibrium during a short embryonic period is sufficient to induce persistent cellular defects and transcriptional alterations, resulting in severe offspring malformations. In conclusion, the SUMO inhibitor TAK981 has teratogenic effects, disrupting normal fetal development and causing congenital disabilities reminiscent of traits observed in UBA2-related syndrome.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151480"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143464911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Versatility of vimentin assemblies: From filaments to biomolecular condensates and back","authors":"Dolores Pérez-Sala,&nbsp;Silvia Zorrilla","doi":"10.1016/j.ejcb.2025.151487","DOIUrl":"10.1016/j.ejcb.2025.151487","url":null,"abstract":"<div><div>Cytoskeletal structures shape and confer resistance to cells. The intermediate filament protein vimentin forms versatile structures that play key roles in cytoskeletal crosstalk, in the integration of cellular responses to a variety of external and internal cues, and in the defense against stress. Such multifaceted roles can be fulfilled thanks to the vast variety of vimentin proteoforms, which in turn arise from the combinations of a myriad of tightly regulated posttranslational modifications. Diverse vimentin proteoforms will differentially shape its polymeric assemblies, underlying vimentin ability to organize in filaments, bundles, squiggles, droplets, cell surface-bound and/or various secreted forms. Interestingly, certain vimentin dots or droplets have been lately categorized as biomolecular condensates. Biomolecular condensates are phase-separated membraneless structures that are critical for the organization of cellular components and play important roles in pathophysiology. Recent findings have unveiled the importance of low complexity sequence domains in vimentin filament assembly. Moreover, several oxidants trigger the transition of vimentin filaments into phase-separated biomolecular condensates, a reversible process that may provide clues on the role of condensates as seeds for filament formation. Revisiting previous results in the light of recent knowledge prompts the hypothesis that vimentin condensates could play a role in traffic of filament precursors, cytoskeletal crosstalk and cellular responses to stress. Deciphering the “vimentin posttranslational modification code”, that is, the structure-function relationships of vimentin proteoforms, constitutes a major challenge to understand the regulation of vimentin behavior and its multiple personalities. This will contribute to unveil essential cellular mechanisms and foster novel opportunities for drug discovery.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151487"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tri-culture model of intestinal epithelial cell, macrophage, and bacteria for the triggering of inflammatory bowel disease on a microfluidic device","authors":"Shiori Tamura ,&nbsp;Clarissa Ellice Talitha Pasang ,&nbsp;Minami Tsuda ,&nbsp;Shilan Ma ,&nbsp;Hiromasa Shindo ,&nbsp;Noriyuki Nagaoka ,&nbsp;Tomoki Ohkubo ,&nbsp;Yoichi Fujiyama ,&nbsp;Miho Tamai ,&nbsp;Yoh-ichi Tagawa","doi":"10.1016/j.ejcb.2025.151495","DOIUrl":"10.1016/j.ejcb.2025.151495","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) involves gastrointestinal inflammation, due to intestinal epithelial barrier destruction caused by excessive immune activation. Conventional cell culture systems do not provide a model system that can recapitulate the complex interactions between epithelial cells, immune cells, and intestinal bacteria. To address this, we developed a microfluidic device that mimics the inflammatory response associated with microbial invasion of the intestinal mucosa. The device consisted of two media channels, an upper and a lower channel, and a porous membrane between these channels on which C2BBe1 intestinal epithelial cells were seeded to form a tight junction layer. Each electrode was placed in contact with both channels to continuously monitor the tight junction state. Fresh medium flow allowed bacterial numbers to be controlled and bacterial toxins to be removed, allowing co-culture of mammalian cells and bacteria. In addition, RAW264 macrophage cells were attached to the bottom of the lower channel. By introducing <em>E. coli</em> into the lower channel, the RAW264 cells were activated and produced TNF-α, successfully recapitulating a culture model of inflammation in which the C2BBe1cell tight junction layer was destroyed. The main structure of the device was initially made of polydimethylsiloxane to facilitate its widespread use, but with a view to introducing anaerobic bacteria in the future, a similar phenomenon was successfully reproduced using polystyrene. When TPCA-1, an IκB kinase 2 inhibitor was added into this IBD culture model, the tight junction destruction was significantly suppressed. The results suggest that this IBD culture model also is useful as a screening system for anti-IBD drugs.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151495"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144117049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combining prelamin A accumulation and oxidative stress: A strategy to target glioblastoma","authors":"Maria Vittoria Marvi ,&nbsp;Camilla Evangelisti ,&nbsp;Camilla Bruna Cerchier ,&nbsp;Antonietta Fazio ,&nbsp;Irene Neri ,&nbsp;Foteini-Dionysia Koufi ,&nbsp;William Blalock ,&nbsp;Vittoria Cenni ,&nbsp;Matteo Zoli ,&nbsp;Sofia Asioli ,&nbsp;Luca Morandi ,&nbsp;Enrico Franceschi ,&nbsp;Lucia Manzoli ,&nbsp;Cristina Capanni ,&nbsp;Stefano Ratti","doi":"10.1016/j.ejcb.2025.151491","DOIUrl":"10.1016/j.ejcb.2025.151491","url":null,"abstract":"<div><div>Glioblastoma is the most aggressive and prevalent tumor of the Central Nervous System (CNS) with limited treatment options and poor patient outcomes. Standard therapies, including surgery, radiation, and chemotherapy, provide only modest survival benefits, highlighting the need for innovative therapeutic approaches. This study investigates a novel strategy targeting prelamin A processing in glioblastoma cells. By inhibiting the farnesyltransferase enzyme using SCH66336 (Lonafarnib), we promote the accumulation of lamin A precursor (prelamin A) in glioblastoma cells, thereby increasing their susceptibility to oxidative stress induced by Menadione administration, while sparing normal human astrocytes. Notably, the combined SCH66336-Menadione treatment reduced cell proliferation, modified the expression of stemness markers, and decreased viability in patient-derived glioblastoma stem cells, which represent the population responsible for tumor aggressiveness and recurrence. These findings indicate that inhibiting prelamin A processing could be a potential strategy to reduce glioblastoma aggressiveness and enhance therapeutic outcomes, particularly for treatment-resistant glioblastoma stem cell populations. This approach shows potential for integrating prelamin A processing disruption as a complementary strategy in glioblastoma therapy.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151491"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143885938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"microRNA-183–5p induces cell density-dependent apoptosis through the regulation of Presenilin 2","authors":"Yuki Yabuuchi ,&nbsp;Yosuke Matsuno ,&nbsp;Kai Yazaki ,&nbsp;Wei Zhen Ting ,&nbsp;Kengo Nishino ,&nbsp;Sosuke Matsumura ,&nbsp;Kenya Kuramoto ,&nbsp;Kazufumi Yoshida ,&nbsp;Masashi Matsuyama ,&nbsp;Takumi Kiwaoto ,&nbsp;Yuko Morishima ,&nbsp;Nobuyuki Hizawa","doi":"10.1016/j.ejcb.2025.151494","DOIUrl":"10.1016/j.ejcb.2025.151494","url":null,"abstract":"<div><div>Cells undergo apoptosis under dense culture condition to maintain homeostasis. Impaired apoptosis may contribute to the excessive accumulation of pathogenetic cells in such diseases as cancer and organ fibrosis. Elucidating the molecular mechanisms regulating cell density-dependent apoptosis may provide novel therapeutic strategy against these diseases. We have reported Notch signaling, activated by γ-secretase under dense culture condition, regulates cell density-dependent apoptosis through the induction of IL-6. Presenilin 2 (PSEN2) is a subunit of γ-secretase and has been shown to modulate apoptosis. The role for PSEN2 in cell density-dependent apoptosis and Notch signaling activation, however, remains unclear. Here, we show a crucial role for PSEN2 in the regulation of cell density-dependent apoptosis in NIH 3T3 cells. PSEN2 protein primarily existed as C-terminal fragment (CTF). PSEN2 CTF expression was upregulated as cell density increased. PSEN2 regulated the development of apoptosis, which is accompanied by increased Bcl-2 expression, decreased Bax expression, and activated PI3K/Akt pathway. PSEN2 is predicted to be targeted by microRNA-183–5p (miR-183–5p) by several algorithms. We verified miR-183–5p directly regulates PSEN2 expression and induces apoptosis. In conclusion, our results demonstrate a crucial role of PSEN2 and its regulation by miR-183–5p in the regulation of cell density-dependent apoptosis.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151494"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human pluripotent stem cell-derived intestinal organoids for pharmacokinetic studies","authors":"Takumi Saito ,&nbsp;Junichiro Amako ,&nbsp;Teruhiko Watanabe ,&nbsp;Nobuaki Shiraki ,&nbsp;Shoen Kume","doi":"10.1016/j.ejcb.2025.151489","DOIUrl":"10.1016/j.ejcb.2025.151489","url":null,"abstract":"<div><div>The human small intestine is essential for orally administered drugs' absorption, metabolism, and excretion. Human induced pluripotent stem cell (hiPSC)-derived intestinal epithelial cells (IECs) offer a useful model for evaluating drug candidate compounds. We previously reported a protocol to generate matured enterocyte-like cells that exhibit P-gp-mediated efflux and cytochrome P450 3A (CYP3A)-mediated metabolism from human iPSCs. However, under the current protocols, generating iPSC-derived intestinal enterocyte-like cells requires a multi-step differentiation procedure and is time-consuming. Recent progress in intestinal organoid (IO) study provides an understanding of the growth factors that enable the maintenance of adult stem cells. Here, we established an easily accessible protocol using a direct 3D cluster culture to derive IOs from hiPSCs (iPSC-IOs) with high self-proliferative ability. The hiPSC-IOs can be propagated for a long-term and maintained capacity to differentiate and can be cryopreserved. Upon seeding on a two-dimensional monolayer, hiPSC-IOs gave rise to the intestinal epithelial cells (IECs) containing mature cell types of the intestine. The hiPSC-IOs-derived IECs contain enterocytes that show CYP metabolizing enzyme and transporter activities and can be used for pharmacokinetic studies.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151489"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galectin-8 drives ERK-dependent mitochondrial fragmentation, perinuclear relocation and mitophagy, with metabolic adaptations for cell proliferation","authors":"Adely de la Peña ,&nbsp;Claudio Retamal ,&nbsp;Francisca Pérez-Molina ,&nbsp;Nicole Díaz-Valdivia ,&nbsp;Francisco Veloso-Bahamondes ,&nbsp;Diego Tapia ,&nbsp;Jorge Cancino ,&nbsp;Felix Randow ,&nbsp;Alfonso González ,&nbsp;Claudia Oyanadel ,&nbsp;Andrea Soza","doi":"10.1016/j.ejcb.2025.151488","DOIUrl":"10.1016/j.ejcb.2025.151488","url":null,"abstract":"<div><div>Mitochondria adapt to the cell proliferative demands induced by growth factors through dynamic changes in morphology, distribution, and metabolic activity. Galectin-8 (Gal-8), a carbohydrate-binding protein that promotes cell proliferation by transactivating the EGFR-ERK signaling pathway, is overexpressed in several cancers. However, its impact on mitochondrial dynamics during cell proliferation remains unknown. Using MDCK and RPTEC kidney epithelial cells, we demonstrate that Gal-8 induces mitochondrial fragmentation and perinuclear redistribution. Additionally, mitochondria adopt donut-shaped morphologies, and live-cell imaging with two Keima-based reporters demonstrates Gal-8-induced mitophagy. ERK signaling inhibition abrogates all these Gal-8-induced mitochondrial changes and cell proliferation. Studies with established mutant versions of Gal-8 and CHO cells reveal that mitochondrial changes and proliferative response require interactions between the N-terminal carbohydrate recognition domain of Gal-8 and α-2,3-sialylated N-glycans at the cell surface. DRP1, a key regulator of mitochondrial fission, becomes phosphorylated in MDCK cells or overexpressed in RPTEC cells in an ERK-dependent manner, mediating mitochondrial fragmentation and perinuclear redistribution. Bafilomycin A abrogates Gal-8-induced cell proliferation, suggesting that mitophagy serves as an adaptation to cell proliferation demands. Functional analysis under Gal-8 stimulation shows that mitochondria maintain an active electron transport chain, partially uncoupled from ATP synthesis, and an increased membrane potential, indicative of healthy mitochondria. Meanwhile, the cells exhibit increased extracellular acidification rate and lactate production via aerobic glycolysis, a hallmark of an active proliferative state. Our findings integrate mitochondrial dynamics with metabolic adaptations during Gal-8-induced cell proliferation, with potential implications for physiology, disease, and therapeutic strategies.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151488"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143800685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in modeling the Charcot-Marie-Tooth disease: Human induced pluripotent stem cell-derived Schwann cells harboring SH3TC2 variants","authors":"Camille Loret ,&nbsp;Camille Scherrer ,&nbsp;Amandine Rovini ,&nbsp;Ioanna Pyromali ,&nbsp;Pierre-Antoine Faye ,&nbsp;Angélique Nizou ,&nbsp;Franck Sturtz ,&nbsp;Frédéric Favreau ,&nbsp;Anne-Sophie Lia","doi":"10.1016/j.ejcb.2025.151485","DOIUrl":"10.1016/j.ejcb.2025.151485","url":null,"abstract":"<div><div>Human induced pluripotent stem cells (hiPSCs) represent a powerful tool for investigating neuropathological disorders, such as Charcot-Marie-Tooth disease (CMT), the most prevalent inherited peripheral neuropathy, where the cells of interest are hardly accessible. Advancing the development of appropriate cellular models is crucial for studying the disease’s pathophysiology. In this study, we present the first two isogenic hiPSC-derived Schwann cell models for studying CMT4C, also known as AR-CMTde-<em>SH3TC2</em>. This subtype of CMT is associated with alterations in <em>SH3TC2</em> and is the most prevalent form of autosomal recessive demyelinating CMT. We aimed to study the impact of two nonsense mutations in <em>SH3TC2</em>. To achieve this, we used two CRISPR hiPSC clones, one carrying a homozygous nonsense mutation: c.211C&gt;T, p.Gln71*, and the other one, carrying the most common AR-CMTde-<em>SH3TC2</em> alteration, c.2860G&gt;A, p.Arg954*. To study the endogenous expression of SH3TC2 in the cells mainly altered in AR-CMTde-<em>SH3TC2</em>, we initiated the differentiation of both our CMT clones and their isogenic control into Schwann cells (SCs). This study represents the first <em>in vitro</em> investigation of human endogenous SH3TC2 expression in AR-CMTde-<em>SH3TC2</em> hiPSC-derived SC models, allowing for the examination of its expression and of its cellular impact. By comparing this AR-CMTde-<em>SH3TC2</em> models to the control one, we observed disparities in RNA and protein expression of SH3TC2. Additionally, our RNA and coculture experiments with hiPSC-derived motor neurons (MNs) revealed delayed maturation of SCs and a reduced ability of SH3TC2-deficient SCs to sustain motor neuron culture. Our findings also demonstrated a disability in receptor recycling in SH3TC2-deficient cells, depending on the AR-CMTde-<em>SH3TC2</em> alteration. These hiPSC-derived-SC models further provide a new modelling tool for studying Schwann cell contribution to CMT4C.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151485"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143705375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Self-organization and applications of neural organoids","authors":"Hideya Sakaguchi","doi":"10.1016/j.ejcb.2025.151496","DOIUrl":"10.1016/j.ejcb.2025.151496","url":null,"abstract":"<div><div>Organoid technology has become a field that attract many researcher’s attention and involvement. “Organoid” is a coined word which means organ like-tissue (Organ+oid), and organoid is determined as stem cell-derived three-dimensional (3D) tissues that recapitulate developmental processes and tissue specific function in vivo. Generally, they are derived from pluripotent stem cells (PSCs) including induced pluripotent stem cells (iPSCs) and embryonic stem cells (ESCs), or from tissue stem cells. The first report that created human 3D cerebral tissue arose in 2008 which is currently considered as the pioneering work of “neural organoid” (Eiraku et al., 2008, Sasai 2013a, Sasai 2013b). The neural organoids provide living human neural tissues that bring opportunities to study human development, human neuroscience, neurological and psychiatric disorders, and evolutions. The neural organoid can be said as “cut &amp; paste” of developmental biological process into a dish. Thus, understanding the background of neural organoid needs developmental knowledge, but current organoid researches looks to use organoid as a tool to study the aim that the researchers want to focus. This leads the organoid research more methodological, and the improvement or sophistication of organoid methods has still been difficult for most of new coming researchers. For this problem, this review provide insights of how to assemble organoid methods from viewpoints of development especially from morphological/structual changes. In this review, I start from the brief history of how neural organoid research emerged from developmental biology. Then I introduce some interesting aspects of neural organoid generation focusing on self-organization of regions and structures. From the viewpoint of a developer of this field, this review also show how to think and adjust the methods to generate novel regional organoids taking hippocampal organoids as an example. Regarding structural self-organization I will introduce cerebral organoid for an example of layer organization in a dish. By showing background knowledge with scientific achievements and interesting aspects, this review will help researchers who want to create novel neural organoids.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151496"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144185230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}