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How Human Induced Pluripotent Stem Cells-Derived Models can Advance our Understanding of Secretion Mechanisms in Physiological and Pathological Contexts? 人类诱导多能干细胞衍生模型如何促进我们对生理和病理背景下分泌机制的理解?
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-10-03 DOI: 10.1111/boc.70035
Lou Fourriere, Gaelle Boncompain

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.

分化细胞的分子结构对确保其特定功能至关重要,并受到膜运输的支持。细胞内组织和/或蛋白质运输中的缺陷导致各种疾病,如神经和心脏疾病。近年来,人类诱导多能干细胞(hiPSCs)已被用于疾病模型。事实上,多能干细胞是揭示分化细胞复杂形态和特化功能的分泌运输途径的组织和功能能力差异的有力模型。这篇综述的重点是对hipsc衍生模型(如神经元和心肌细胞)的膜运输机制、调控和缺陷进行研究的必要性,并强调了这些模型在揭示细胞类型特异性特性方面的强大作用。在hipscs衍生的模型中进行的一些研究可以解释病理条件下的贩运缺陷。基因组编辑、细胞内工具、高分辨率显微镜和快速成像的新进展对于研究hipsc中的膜运输至关重要,这些将被讨论,以及它们目前的局限性和改进领域。总之,这篇综述旨在为相互关联的比较研究铺平道路,这些研究需要了解健康和疾病中调节蛋白质转运的机制。
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引用次数: 0
Membrane Bound E-Cadherin Stimulates PI3K/Akt Signaling 膜结合E-Cadherin刺激PI3K/Akt信号传导。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-10-03 DOI: 10.1111/boc.70034
Aurora Candelario-Martínez, Mónica Vizcarra-Soto, Nicolás Villegas-Sepúlveda, Porfirio Nava

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.

细胞连接蛋白在调节包括增殖和凋亡在内的关键生理过程中起关键作用。e -钙粘蛋白是粘附连接的重要组成部分,通过调节细胞的粘附和增殖来维持肠上皮的稳态。在本研究中,我们探讨了E-cadherin在肠上皮细胞中的功能。我们的研究结果表明,在结肠炎期间,e -钙粘蛋白仍然与结肠炎细胞的细胞膜相关。此外,通过体外系统,我们证明了在结落细胞中,E-cadherin抑制细胞增殖和β-catenin信号传导,同时激活PI3K/Akt通路。提示E-cadherin可抑制结肠炎小鼠结肠细胞增殖,同时促进PI3K/Akt信号通路。
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引用次数: 0
Recombinant Human Fibronectin Mediates Macrophage Polarization via NF-κB/TGF-β1 Pathway to Enhance Fibroblast Proliferation 重组人纤维连接蛋白通过NF-κB/TGF-β1通路介导巨噬细胞极化促进成纤维细胞增殖
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-09-17 DOI: 10.1111/boc.70025
Zongbao Zuo, Zizheng Yang, Jun Zhao, Lei Han, Jing Yang, Yueping Wang, Ziyun Zhang, Daoping Zhou

Objective

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.

Methods

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.

Results

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.

Conclusion

RhFN modulates macrophage polarization through NF-κB inhibition and promotes fibroblast proliferation, adhesion, and migration via TGF-β1/Smad2/3 signaling.

目的:本研究旨在探讨重组人纤维连接蛋白(rhFN)通过核因子κB (NF-κB)/转化生长因子β1 (TGF-β1)信号通路调控巨噬细胞极化进而影响成纤维细胞增殖的分子机制。方法:用LPS激活巨噬细胞RAW 264.7,然后用rhFN处理巨噬细胞,然后用流式细胞术评估巨噬细胞极化。采用酶联免疫吸附法(ELISA)检测白细胞介素(IL)-10、肿瘤坏死因子α (TNF-α)、IL-6、Arg-1及TGF-β1的细胞因子水平。用巨噬细胞条件培养基(CM)培养成纤维细胞NIH 3T3,用CCK-8、细胞粘附和伤口愈合试验评估其增殖、粘附和迁移能力。Western blot检测TGF-β1/Smad2/3、NF-κB信号通路相关蛋白的变化。结果:RhFN显著促进巨噬细胞M2极化,增加TGF-β1分泌,降低促炎细胞因子TNF-α、IL-6,升高IL-10、Arg-1水平。用rhfn处理的巨噬细胞- cm培养成纤维细胞显示Smad2/3磷酸化增加,导致增殖、粘附和迁移能力改善。NF-κB信号的抑制促进了抗炎巨噬细胞的分布,而NF-κB的激活部分逆转了rhFN对成纤维细胞功能的影响。抑制TGF-β1导致成纤维细胞增殖、粘附和迁移能力降低,证实了其在rhfn介导的作用中的关键作用。结论:RhFN通过抑制NF-κB调控巨噬细胞极化,并通过TGF-β1/Smad2/3信号通路促进成纤维细胞增殖、粘附和迁移。
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引用次数: 0
DeepSCEM: A User-Friendly Solution for Deep Learning-Based Image Segmentation in Cellular Electron Microscopy DeepSCEM:细胞电子显微镜中基于深度学习的图像分割的用户友好解决方案
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-09-01 DOI: 10.1111/boc.70032
Cyril Meyer, Victor Hanss, Etienne Baudrier, Benoît Naegel, Patrick Schultz

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.

使用卷积神经网络的深度学习方法在自动图像分割任务中非常有效,细胞电子显微图也不例外。然而,缺乏专用的易于使用的工具在很大程度上减少了这些技术的广泛使用。在这里,我们介绍了DeepSCEM,这是一个使用深度学习对细胞电子显微镜图像进行快速有效分割的简单工具,特别侧重于高效和用户友好的细胞器分割模型的生成和训练。
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引用次数: 0
The Synchrony of STARD4-AS1 and H19 Downregulation with Cardiomyocytes Cell Cycle Arrest STARD4-AS1和H19下调与心肌细胞周期阻滞的同行性
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-08-24 DOI: 10.1111/boc.70028
Mahshad Shiri, Fatemeh Movahedi, Fatemeh Etezadi, Iman Bhia, Eberhard Korsching, Kai Wang, Sedigheh Gharbi, Sara Pahlavan

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.

出生后心肌细胞的永久性细胞周期阻滞阻碍了心脏再生,导致损伤后代偿性纤维化和心功能受损。虽然细胞周期调节蛋白的作用已被充分了解,但长链非编码rna (lncRNAs)的影响仍不清楚。为了解决这一差距,我们重新分析了比较产前和产后心室心肌细胞的公共转录组数据集。计算机分析鉴定了差异表达的lncrna,并选择了四个候选lncrna进行进一步验证。将人胚胎干细胞(hESCs)分化为心肌细胞,并在第10、20和30天评估其细胞周期状态。在增殖性(第10天)和非增殖性(第20天和第30天)hesc来源的心肌细胞(类似于产前和产后心室心肌细胞)中评估硅鉴定的lncRNAs的表达。在候选基因中,STARD4-AS1和H19在硅和体外实验中均表现出永久性下调模式。STARD4-AS1和H19 lncrna可能存在于心肌细胞周期阻滞的调控网络中,并作为心脏再生策略的靶点。
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引用次数: 0
SOX15 Transcriptionally Decreases the Level of MMP2 and Inhibits Vasculogenic Mimicry to Slow Down the Progression of Ovarian Cancer SOX15通过转录降低MMP2水平和抑制血管生成模拟来减缓卵巢癌的进展
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-08-20 DOI: 10.1111/boc.70031
Xiaodan Zhao, Xinjia Wang, Chao Wang, Huiyu Tian, Yang Zhou, Lihong Gong

Background Information

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.

Results

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.

Conclusions

Our results indicate that SOX15 transcriptionally represses MMP2 expression, thereby inhibiting VM formation and ultimately suppressing OV cancer initiation and progression.

Significance

We establish a theoretical foundation for developing novel therapeutic approaches targeting the SOX15/MMP2 axis in OV cancer treatment.

背景信息血管拟态(Vascular mimmimi, VM)是促进卵巢癌患者肿瘤细胞增殖和侵袭的关键机制。性别决定区Y-box 15 (SOX15)抑制肿瘤细胞的恶性生长。然而,SOX15在OV癌中的功能尚不明确。利用SKOV-3和ES2细胞系以及裸鼠异种移植模型,我们研究了SOX15对OV癌肿瘤细胞生长和VM形成的影响及其潜在机制。结果SOX15能抑制SKOV-3细胞的增殖、迁移和侵袭。SOX15过表达减少了SKOV-3细胞中VM的形成,同时VE-cadherin和血管内皮生长因子A (VEGFA)水平降低。同样,SOX15抑制ES2细胞的增殖和运动。此外,异种移植实验表明,SOX15敲低会增加小鼠的肿瘤体积,同时上调Ki67和基质金属蛋白酶2 (MMP2)在肿瘤组织中的表达。CD31/PAS双染色显示,沉默SOX15可促进肿瘤中VM的形成。从机制上讲,SOX15过表达在mRNA和蛋白水平上下调MMP2,抑制VM形成,从而减缓OV癌症进展。双荧光素酶报告基因检测显示,SOX15过表达抑制MMP2启动子活性,染色质免疫沉淀PCR (ChIP-PCR)证实SOX15与MMP2启动子直接结合。结论SOX15通过转录抑制MMP2的表达,从而抑制VM的形成,最终抑制OV癌的发生和进展。意义为开发靶向SOX15/MMP2轴的OV肿瘤治疗新方法奠定了理论基础。
{"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}
引用次数: 0
PU.1 Facilitates Endothelial-to-Mesenchymal Transition in Cardiac Endothelial Cells PU.1促进心脏内皮细胞向间质转化
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-07-28 DOI: 10.1111/boc.70029
Ran Meng, Bin Huang, Fan Yang, Nannan Zhang, Bin Feng, Dalong Zhu

Background: 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.

Methods: 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).

Results: 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.

Conclusion: 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.

背景:内皮-间充质转化(EndMT)在心脏纤维化的发病机制中起关键作用。然而,驱动EndMT的分子机制仍然知之甚少。本研究利用原代心脏内皮细胞研究转录因子PU.1在EndMT中的调控作用。方法:采用免疫荧光法测定培养细胞的特征蛋白标志物。通过siRNA转染实现PU.1的敲低。在mRNA和蛋白水平上定量分析关键基因的表达。通过迁移和管形成分析来评估EndMT的进展。此外,利用免疫沉淀检测PU.1与磷酸化Smad3 (p-Smad3)的相互作用。结果:TGF-β1诱导的EndMT伴PU.1表达显著上调。PU.1沉默可减弱EndMT,在TGF-β1刺激下CD31/VE-cadherin升高,α-SMA/N-cadherin/FSP-1水平降低。PU.1的敲除在功能上损害了细胞的迁移,同时促进了血管的管腔形成。相反,在心脏内皮细胞中,强迫PU.1表达足以驱动EndMT。在机制上,我们的数据表明PU.1可能通过直接结合和稳定p-Smad3蛋白来增强Smad3的磷酸化。结论:PU.1通过增强Smad3磷酸化和稳定性来驱动心脏内皮细胞的EndMT。这些结果阐明了EndMT的新分子途径,并确定了PU.1作为减轻心脏纤维化的潜在治疗靶点。
{"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}
引用次数: 0
The Chronological Trigger: The Orchestra Between Homeobox Genes and the Circadian Clock During Development 时间触发器:在发育过程中同源盒基因和生物钟之间的管弦乐队
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-07-25 DOI: 10.1111/boc.70027
Joice de Faria Poloni, Bruno César Feltes

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.

作为胚胎发育的主要调控者,调控同型盒基因是发育生物学的基础。尽管关于微调同源盒基因表达的话题越来越多,但关于昼夜节律如何影响其控制以及反之亦然的讨论仍然需要改进。由于生物钟的内在重要性及其对包括发育和妊娠在内的几种分子机制的影响,这一机制与同源盒基因之间的相互作用成为一个有意义的讨论。这项工作旨在回顾和批判性地讨论在多种生物中同源盒基因和昼夜节律调节之间的串扰,重点是分化和发育机制。对该主题的新观点给予了相当大的关注。
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引用次数: 0
Meeting Report on the Symposium Organized to Celebrate the 40th Anniversary of the French Society for Cell Biology 庆祝法国细胞生物学学会成立40周年研讨会会议报告
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-07-16 DOI: 10.1111/boc.70014
Florence Niedergang, Renaud Chabrier, Isabelle Tardieux

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.

法国细胞生物学学会(SBCF)聚集了在细胞生物学广泛领域工作的所有研究人员,并积极参与若干任务。事实上,从交流最新的突破到宣布即将到来的活动,SBCF还发现和培养新兴人才,同时资助年轻研究人员帮助他们参加科学会议。该协会的使命是促进科学领域的发展,促进知识的传播,并在国际舞台上成为法国细胞生物学研究的参考。在此背景下,SBCF与全球细胞生物学学会建立了知识和专业知识网络,并继续通过国际会议的联合会议促进伙伴关系。同样,自2022年以来,SBCF一直在组织一年一度的主题国际研讨会,名为“……的细胞生物学”,以聚焦感兴趣的特定主题。过去的版本突出了冠状病毒、神经元和植物等主题,展示了该学科的广泛范围。除了这些科学活动外,SBCF还非常致力于支持和定期组织各种活动,以提高公众对科学,特别是细胞生物学的认识,并使其参与科学的奇迹。
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引用次数: 0
Dynamic Organization of Cells in Colonic Epithelium is Encoded by Five Biological Rules 结肠上皮细胞的动态组织是由五个生物学规则编码的
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2025-07-14 DOI: 10.1111/boc.70017
Bruce M. Boman, Thien-Nam Dinh, Keith Decker, Brooks Emerick, Shirin R. Modarai, Lynn M. Opdenaker, Jeremy Z. Fields, Christopher Raymond, Gilberto Schleiniger

Tissue organization is fundamental to the form and function of most, if not all, multicellular organisms. But what specifies the precise histologic organization of cells in tissues of plants and animals is unclear. We hypothesize that a tissue code exists that is the basis for dynamic maintenance of tissue organization. Any code for tissue organization must account for how the dynamics of tissue renewal maintain histologic structure. Accordingly, we modeled the dynamics of crypt renewal to determine how the organization of cells is maintained in colonic epithelium. Specifically, we modeled spatial and temporal asymmetries of cell division and established that five simple mathematical laws ([1] timing of cell division, [2] temporal order of cell division, [3] spatial direction of cell division, [4] number of cell divisions, and [5] cell lifespan) constitute a set of biological rules for colonic epithelia. Our results indicate that these rules form the basis of precise organization of cells in colonic epithelium during continuous crypt renewal. These five laws might even provide a means to understand the mechanisms that underlie organization of other tissue types, and how genetic alterations cause tissue disorganization that leads to birth defects and tissue pathology like cancer.

组织是大多数(如果不是全部的话)多细胞生物的形式和功能的基础。但是,是什么具体规定了植物和动物组织中细胞的精确组织学组织尚不清楚。我们假设存在一个组织代码,它是组织组织动态维护的基础。任何组织编码都必须考虑到组织更新的动态如何维持组织结构。因此,我们模拟了隐窝更新的动力学,以确定结肠上皮中细胞的组织是如何维持的。具体来说,我们对细胞分裂的时空不对称性进行了建模,并建立了5个简单的数学规律([1]细胞分裂时间、[2]细胞分裂时间顺序、[3]细胞分裂空间方向、[4]细胞分裂次数和[5]细胞寿命)构成了一套结肠上皮的生物学规律。我们的研究结果表明,这些规则构成了在连续隐窝更新过程中结肠上皮细胞精确组织的基础。这五条定律甚至可能提供一种方法来理解其他组织类型的组织机制,以及基因改变如何导致组织紊乱,从而导致出生缺陷和癌症等组织病理。
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引用次数: 0
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