Angiogenesis最新文献

{"title":"Micropuncture and granular hydrogel scaffolds to surgically bioengineer a perfusable and stably patterned microvasculature","authors":"Jessica C. El-Mallah,&nbsp;Zaman Ataie,&nbsp;Summer N. Horchler,&nbsp;Mary E. Landmesser,&nbsp;Mohammad Hossein Asgardoon,&nbsp;Olivia Waldron,&nbsp;Arian Jaberi,&nbsp;Alexander Kedzierski,&nbsp;Mingjie Sun,&nbsp;Amir Sheikhi,&nbsp;Dino J. Ravnic","doi":"10.1007/s10456-025-10003-x","DOIUrl":"10.1007/s10456-025-10003-x","url":null,"abstract":"<div><p>Vascularization of implanted biomaterials is critical to reconstructive surgery and tissue engineering. Ultimately, the goal is to promote a rapidly perfusable hierarchical microvasculature that persists with time and can meet underlying tissue needs. We have previously shown that using a microsurgical technique, termed micropuncture (MP), in combination with porous granular hydrogel scaffolds (GHS) fabricated via interlinking hydrogel microparticles (microgels) results in a rapidly perfusable patterned microvasculature. However, whether this engineered microvasculature remains stable at longer time points remains unknown. Here, we combine MP with GHS and compare overall microvascular architecture and phenotype along with the evolving cellular landscape over a 28 day period. We demonstrate perfusable patterned microvascular stability in our MP + GHS model that occurs alongside a sustained rise in endothelial cell and macrophage recruitment. Specifically, MP yields a significant rise in M2 macrophages between the 7 and 28 day time points, suggesting ongoing microvascular remodeling, even in the presence of early pericyte stabilization. With time, the GHS microvasculature acquires a relatively equivalent arterial and venous morphology, as assessed through Ephrin-B2 and EphB4 quantification. Finally, angiography at 28 days shows that MP + GHS is associated with more perfusable microvascular loops when compared with MP + Bulk (nonporous) scaffolds. Hence, our surgically bioengineered microvasculature offers a unique opportunity to sustainably and precisely control biomaterial vascularization and ultimately advance the fields of reconstructive surgery and tissue engineering.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":""},"PeriodicalIF":9.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-025-10003-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145021570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vasculogenic potential of adipose tissue derived stem cells from patients with chronic spinal cord injury and pressure injuries","authors":"Ángela Santos-De-La-Mata,&nbsp;Pedro F. Esteban,&nbsp;Mario Martínez-Torija,&nbsp;Beatriz Paniagua-Torija,&nbsp;Fa. Javier Espino-Rodríguez,&nbsp;Lucía Beltrán-Camacho,&nbsp;Celia Camacho-Toledano,&nbsp;Mónica Alcobendas-Maestro,&nbsp;Fernando García-García,&nbsp;Eduardo Molina-Holgado,&nbsp;Ma Carmen Durán-Ruiz,&nbsp;Juan M. Melero-Martin,&nbsp;Rafael Moreno-Luna","doi":"10.1007/s10456-025-10002-y","DOIUrl":"10.1007/s10456-025-10002-y","url":null,"abstract":"<div><p>Limited vascularization and ischemia are major contributors to the chronicity of wounds, such as ulcers and traumatic injuries, which impose significant medical, social, and economic burdens. These challenges are particularly pronounced in patients with spinal cord injury (SCI), a disabling condition associated with vascular dysfunction, infections, and impaired peripheral circulation, complicating the treatment of pressure injuries (PIs) and the success of reconstructive procedures like grafts and flaps. Regenerative medicine aims to address these issues by identifying effective cellular therapies to restore vascular beds. Among these, cells from the stromal vascular fraction (SVF) of adipose tissue (AT) are promising due to their abundance of angiogenic and vasculogenic cells, including mesenchymal stem cells (MSCs) and endothelial colony-forming cells (ECFCs). This study evaluated the vasculogenic potential of AT-derived cellular fractions isolated via enzymatic digestion of white adipose tissue (WAT). We compared adipose-derived stem cells (ASCs) cultured from SVF with a combination of ECFCs and MSCs, expanded separately and transplanted in a 40:60 ratio. Results showed that while ASCs promote angiogenesis and vasculogenesis, the ECFC/MSC combination is superior, consistently forming perfused vascular beds in subcutaneous implants in nude mice. Furthermore, ECFCs and MSCs extracted from small amounts of WAT in SCI patients with PIs demonstrated similar functionality and vasculogenic potential to cells from healthy controls. These findings highlight the potential of AT-derived ECFCs and MSCs in autologous cell therapies, offering a promising avenue for advancing vascular regeneration in patients with SCI.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":""},"PeriodicalIF":9.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-025-10002-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145021569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial transfer from adipose-derived regenerative cells contributes therapeutic angiogenesis in a murine hindlimb ischemia model","authors":"Yiyang Che,&nbsp;Yuuki Shimizu,&nbsp;Takumi Hayashi,&nbsp;Junya Suzuki,&nbsp;Zhongyue Pu,&nbsp;Kazuhito Tsuzuki,&nbsp;Shingo Narita,&nbsp;Yoshimitsu Yura,&nbsp;Rei Shibata,&nbsp;Toyoaki Murohara","doi":"10.1007/s10456-025-10001-z","DOIUrl":"10.1007/s10456-025-10001-z","url":null,"abstract":"<div><h3>Objective</h3><p>Adipose-derived regenerative cells (ADRCs) are promising cell sources for damaged tissue regeneration. The efficacy of therapeutic angiogenesis with ADRC implantation in patients with critical limb ischemia has been demonstrated in clinical studies. There are several possible mechanisms in this process such as cytokines and microRNA. Recently, cell-to-cell transfer of mitochondria gains more attention in regenerative medicine. However, the role of the mitochondrial transfer mechanism in ADRCs in the regeneration of functional tissue perfusion following ischemic injury remains unclear. In this study, we aimed to investigate whether mitochondrial transfer is a potential mechanism of therapeutic angiogenesis in ADRCs using a murine hindlimb ischemia model.</p><h3>Methods and results</h3><p>In initial studies, the occurrence of mitochondrial transfer of ADRC to endothelial cells and macrophages in a series of pro-angiogenic effects of ADRC was demonstrated in a mouse model of hindlimb ischemia. Subsequently, we comprehensively elucidated the modes of mitochondrial transfer from ADRCs to HUVECs and macrophages mediated by Connexin43-based gap junctions and tunneling nanotubes using time-lapse confocal microscopy and cell sorting techniques. Furthermore, mitochondrial transfer from ADRCs enhanced mitochondrial biogenesis and angiogenesis in vascular endothelial cells and shifted macrophages toward the M2-phenotype. Notably, partially canceled mitochondrial transfer from ADRCs could impede the angiogenic ability of ADRCs in hind limb ischemia.</p><h3>Conclusions</h3><p>ADRCs can protect against ischemic limbs, at least in part by mitochondrial transfer via gap junctions and tunneling of nanotubes into injured endothelial cells and macrophages. Additionally, mitochondrial transfer is a potential mechanism for therapeutic angiogenesis with ADRCs in hindlimb ischemia.</p><h3>Graphical abstract</h3><p>Schematic illustration showing potential mechanisms of mitochondrial transfer from ADRCs in mouse hindlimb ischemia model. This figure was created with BioRender.</p><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":""},"PeriodicalIF":9.2,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-025-10001-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145021571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G3BP1 maintains endothelial barrier integrity through dual mechanisms: direct stabilization of junction protein mRNAs and suppression of the inflammatory MYD88-ARNO-ARF6 pathway","authors":"Weiyue Sun,&nbsp;Haoran Wu,&nbsp;Yuxi He,&nbsp;Huiqiao Chen,&nbsp;Yuanhui Meng,&nbsp;Guofang Tang,&nbsp;Jinshun Zhu,&nbsp;Zhengwang Wen,&nbsp;Hui Zhang,&nbsp;Rongzhou Wu,&nbsp;Guowei Wu,&nbsp;Chunxiang Zhang,&nbsp;Maoping Chu,&nbsp;Bin Wen","doi":"10.1007/s10456-025-09993-5","DOIUrl":"10.1007/s10456-025-09993-5","url":null,"abstract":"<div><p>Vascular permeability, crucial for organ function, relies on the endothelial barrier formed by intercellular junctions (AJs, TJs). However, mechanisms regulating these junctions and maintaining endothelial barrier integrity are incompletely understood. Here, we investigate the RNA-binding protein G3BP1’s role in endothelial barrier integrity using <i>G3bp1</i> knockout mice and <i>G3BP1</i>-deficient human endothelial cells. We found that G3BP1 loss compromised barrier function, leading to reduced AJ and TJ protein levels and increased vascular permeability, particularly under LPS-induced inflammatory conditions. Mechanistically, G3BP1 exerts dual post-transcriptional control: it directly binds to and stabilizes mRNAs of key AJ proteins (VE-cadherin, p120), ensuring their sustained expression. Concurrently, G3BP1 binds MYD88 mRNA and promotes its decay, thereby suppressing the pro-permeability MYD88-ARNO-ARF6 signaling cascade, particularly during inflammation. Pharmacological or genetic inhibition of this pathway, or VE-cadherin overexpression, partially rescued barrier defects in G3BP1-deficient models, with combined interventions showing enhanced restoration under inflammatory conditions. Our findings reveal that G3BP1 maintains vascular barrier integrity through dual post-transcriptional control: stabilizing key AJ mRNA and suppressing inflammatory signaling via MYD88 mRNA decay. Targeting G3BP1 may offer a therapeutic strategy for vascular permeability disorders.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":""},"PeriodicalIF":9.2,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144897189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiology of endothelial dysfunction in Fontan circulation: from bench to bedside and back again","authors":"Amalia Baroutidou,&nbsp;Artemios G. Karagiannidis,&nbsp;Theodoros Dimitroulas,&nbsp;Vasileios Kamperidis,&nbsp;Antonios Ziakas,&nbsp;Konstantinos Dimopoulos,&nbsp;George Giannakoulas","doi":"10.1007/s10456-025-09996-2","DOIUrl":"10.1007/s10456-025-09996-2","url":null,"abstract":"<div><p>The Fontan procedure is a definitive surgical approach for complex cardiac malformations, redirecting systemic venous blood into the pulmonary circulation through a staged repair that separates systemic and pulmonary venous returns in the absence of a subpulmonary ventricle. The ensuing unique hemodynamic conditions compromise the endothelial function both in the pulmonary and the systemic circulation. The underlying pathophysiological mechanisms, although distinct within each vascular bed, are interrelated and may collectively contribute to progressive end-organ dysfunction, ultimately accounting for the significant morbidity burden in Fontan patients. This review provides an overview of the current knowledge on the pathophysiology of pulmonary and systemic vasculopathy in Fontan circulation, with particular emphasis on the interplay between endothelial dysfunction and adverse clinical outcomes. Remaining gaps in knowledge and directions of future research are also discussed.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":""},"PeriodicalIF":9.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10456-025-09996-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MY-1 promotes angiogenesis in the ischemic hindlimbs by regulating the stability of CDC42 via PSMD14","authors":"Xian Ding,&nbsp;Yuxin Zhang,&nbsp;Yuting Zeng,&nbsp;Qianlin Li,&nbsp;Sijie Qiu,&nbsp;Ping Xiao,&nbsp;Xin Luo,&nbsp;Jiaping Chen,&nbsp;Qianwen Deng,&nbsp;Dehong Yang,&nbsp;Yanli Zhang,&nbsp;Wenjuan Yan","doi":"10.1007/s10456-025-09989-1","DOIUrl":"10.1007/s10456-025-09989-1","url":null,"abstract":"<div><p>Critical limb ischemia (CLI) is a refractory peripheral artery disease characterized by tissue ischemia, presenting significant therapeutic challenges. Current surgical revascularization treatments are limited by indications, complications, and other constraints, making the identification of novel therapeutic strategies an important objective for CLI management. In this study, we designed and synthesized a novel short peptide, named MY-1, and developed a GelMA/MY-1 hydrogel sustained-release system for local application in a mouse hindlimb ischemia model. This system significantly promoted blood flow reperfusion and muscle tissue repair in the ischemic region. In vitro experiments revealed that MY-1 promoted the formation of filopodia in endothelial cells, accelerating cell migration and confirming the critical role of CDC42 in this process. Importantly, we found that MY-1 regulates the stability of CDC42, driving endothelial cell dynamics. Building on this, we identified PSMD14 as a novel upstream target influencing CDC42 stability. Silencing PSMD14 impaired filopodia formation, migration ability, and CDC42 stability in endothelial cells, and MY-1 could not reverse these effects. This indicates the potential of MY-1 in regulating deubiquitinase activity in angiogenesis.</p></div>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":""},"PeriodicalIF":9.2,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144868915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RE: acute aortic dissection in a patient with hereditary hemorrhagic telangiectasia associated with juvenile polyposis due to SMAD4 mutation.","authors":"Ehab Y Harahsheh, George Bcharah, Misha B Asif, Linnea M Baudhuin, Pavel Pichurin, Fadi Shamoun, Mayowa A Osundiji","doi":"10.1007/s10456-025-09999-z","DOIUrl":"https://doi.org/10.1007/s10456-025-09999-z","url":null,"abstract":"","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":"41"},"PeriodicalIF":9.2,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiopoietin-2 binds to FGFR2, inhibits FGF-FGFR2 signaling, and delays cutaneous wound healing by inhibiting wound angiogenesis.","authors":"Minji Sim, Hidetaka Ohnuki, Stewart Durell, Haydar Bulut, Yuyi Wang, Marzena Dyba, Sergey G Tarasov, Lisa M Jenkins, Giovanna Tosato","doi":"10.1007/s10456-025-09988-2","DOIUrl":"10.1007/s10456-025-09988-2","url":null,"abstract":"<p><p>Wound healing is an essential repair process, and impaired wound healing is a common and sometimes debilitating medical problem. Despite advances in wound healing approaches, optimal management strategies are lacking, partly due to an incomplete understanding of the complex pathophysiology of this process. Here we show that Ang2, a previously known ligand for the Tie2 receptor, also binds to fibroblast growth factor receptor 2 (FGFR2) independently of Tie2 and attenuates FGF/FGFR2 signaling in endothelial cells. Functionally, Ang2 inhibits endothelial cell migration induced by FGF. In mouse, topical Ang2 delays the healing of skin wounds, associated with reduced wound angiogenesis and recruitment of mesenchymal-type cells. Additionally, topical AMG386, a blocker of Ang1/Ang2 binding to Tie2 and systemic REGN910, a blocker of Ang2 binding to Tie2, accelerate wound repair, associated with increased wound angiogenesis and recruitment of inflammatory cells. These results identify the tyrosine kinase FGFR2 as a previously unrecognized Ang2 receptor, explaining some of the context-dependent functions of Ang2 in endothelial cells. Since Ang2 is induced in cutaneous wounds and endogenous FGF/FGFR2 is essential for wound repair, Ang2 blockade holds promise as a new evidence-based therapeutic option to promote wound repair.</p>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":"43"},"PeriodicalIF":9.2,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UHRF1 in endothelial cells is essential for angiogenesis and associated with the activation of pro-angiogenic signaling pathways and expression of endothelial genes.","authors":"Ying Liu, Jiake Mo, Zi Guo, Jiaqi Zhang, Weian Tang, Xubiao Meng, Yufang Luo, Fang Wang, Zhaohui Mo","doi":"10.1007/s10456-025-09998-0","DOIUrl":"https://doi.org/10.1007/s10456-025-09998-0","url":null,"abstract":"<p><p>Epigenetics is increasingly recognized as a crucial factor in angiogenesis. Ubiquitin-like with PHD and RING Finger Domains 1 (UHRF1) is an important epigenetic regulatory protein involved in regulating cellular life processes, developing many diseases. However, its potential role in regulating embryonic vascular development and postnatal angiogenesis is unclear. Our study found that endothelial cell-specific UHRF1 knockout mice showed obvious developmental disorders at the embryonic stage (E11.5-15.5), including impaired development of the individual embryo size and organs, sparse vascularity in the yolk sac, or even death. In the lower limb ischemia model, UHRF1 expression in ischemic muscle tissues of mice is proportionate to the regeneration of blood vessels. To confirm the specific inhibition of UHRF1, we transfected an adeno-associated virus serotype 9 which inserted a TIE-2 promoter and mediated the delivery of short hairpin RNA (AAV9-TIE-2-shUHRF1) into mouse vascular endothelial cells to knock down UHRF1 specifically. We observed that the knockdown of UHRF1 in endothelial cells results in poorer lower limb perfusion in mice. Mechanically, UHRF1 knockdown decreased the tube-forming capacity of ECFCs, whereas overexpression of UHRF1 by diabetic ECFCs where UHRF1 expression is typically downregulated significantly increased the tube-forming capacity of the cells. RNAseq and related bioinformatics analyses showed that differentially expressed genes (DEGs) were mainly involved in angiogenesis-related pathways. The results of qPCR and western blot showed that the protein and mRNA levels of angiogenesis-related factors (VEGF, PDGF, and ANGPT1), as well as vascular endothelial surface marker molecules (VEGFR2, CD31, and c-Kit), were down-regulated accordingly. Furthermore, ChIP experiments showed that UHRF1 was able to bind the promoters of VEGFR2 and CD31, affecting the levels of histone-methylated protein (H3K4me3 and H3K27me3) enriched in the promoter region. However, the expression of CD31 and VEGFR2 can be reversed separately after the transformation of different histone-methylated protein levels (H3K4me3 and H3K27me3). Taken together, UHRF1 may regulate angiogenic gene expression and vascular endothelial cell differentiation through epigenetic mechanisms and is essential for angiogenesis.</p>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 4","pages":"42"},"PeriodicalIF":9.2,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo profiling of the endothelium using 'AngioTag' zebrafish.","authors":"Mayumi F Miller, Leah J Greenspan, Derek E Gildea, Kathryn Monzo, Gennady Margolin, Van N Pham, Keith K Ameyaw, Lisa Price, Natalie Aloi, Amber N Stratman, Andrew E Davis, Isabella Cisneros, Caleb A Mertus, Ryan K Dale, Andreas D Baxevanis, Brant M Weinstein","doi":"10.1007/s10456-025-09990-8","DOIUrl":"10.1007/s10456-025-09990-8","url":null,"abstract":"<p><p>Vascular endothelial cells in vivo are exquisitely regulated by their local environment, which is disrupted or absent when using methods such as FACS sorting of cells isolated from animals or in vitro cell culture. Here, we profile the gene expression patterns of undisturbed endothelial cells in living animals using a novel \"AngioTag\" zebrafish transgenic line that permits isolation of actively translating mRNAs from endothelial cells in their native environment. This transgenic line uses the endothelial cell-specific kdrl promoter to drive expression of an epitope tagged Rpl10a 60 S ribosomal subunit protein, allowing for Translating Ribosome Affinity Purification (TRAP) of actively translating endothelial cell mRNAs. By performing TRAP-RNAseq on AngioTag animals, we demonstrate strong enrichment of endothelial-specific genes and have uncovered both novel endothelial genes and unique endothelial gene expression signatures for different adult organs. Finally, we generated a versatile \"UAS: RiboTag\" transgenic line to allow a wider array of different zebrafish cell and tissue types to be examined using TRAP-RNAseq methods. These new tools offer an unparalleled resource to study the molecular identity of cells in their normal in vivo context.</p>","PeriodicalId":7886,"journal":{"name":"Angiogenesis","volume":"28 3","pages":"40"},"PeriodicalIF":9.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12227374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144558871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}