ArticleScientific reports2016
Activated Stat5 trafficking Via Endothelial Cell-derived Extracellular Vesicles Controls IL-3 Pro-angiogenic Paracrine Action.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 80 citations in OpenAlex.
- Percutaneous Coronary Intervention (PCI) Reprograms Circulating Extracellular Vesicles from ACS Patients Impairing Their Cardio-Protective Properties.International journal of molecular sciences · 2021Trial
- Mapping the miRNA landscape of primitive macrophage extracellular vesicles highlights their pro-vasculogenic effects in engineered human cardiac tissue.APL bioengineering · 2026Article
- Proangiogenic Properties of Extracellular Vesicles Secreted by Endothelial Cells Reversibly Primed for Anoikis: A Possible Autocrine Mechanism Induced by Astrocytoma Extracellular Matrix.International journal of molecular sciences · 2026Article
- Fueling the Seed: Growth Factors and Cytokines Driving Cancer Stem Cells in Gynecological Malignancies.International journal of molecular sciences · 2025Review
- Roles and Potential Mechanisms of Endothelial Cell-Derived Extracellular Vesicles in Ischemic Stroke.Translational stroke research · 2025Review
- Chronic Stress-Induced and Tumor Derived SP1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Monocyte/macrophage-derived IL-15 activates STAT5 to trigger the EFNA1/NCOA2-positive feedback loop, facilitating retinal angiogenesis in high-glucose environments.Molecular vision · 2025Article
- Article
- Endothelial extracellular vesicles enhance vascular self-assembly in engineered human cardiac tissues.Biofabrication · 2024Article
- The role of the hematopoietic stem/progenitor cells-derived extracellular vesicles in hematopoiesis.Heliyon · 2024Article
- Circulating extracellular vesicles as biomarkers in the diagnosis, prognosis and therapy of cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Acquisition of drug resistance in endothelial cells by tumor-derived extracellular vesicles and cancer progression.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Role of exosomal ncRNAs in traumatic brain injury.Non-coding RNA research · 2023Review
- Extracellular Vesicles fromInternational journal of molecular sciences · 2022Article
- Extracellular Vesicles in Multiple Myeloma-Cracking the Code to a Better Understanding of the Disease.Cancers · 2022Review
- The microenvironment-a general hypothesis on the homeostatic function of extracellular vesicles.FASEB bioAdvances · 2022Article
- Exosomes in cardiovascular diseases: a blessing or a sin for the mankind.Molecular and cellular biochemistry · 2022Review
- PFKFB4 promotes angiogenesis via IL-6/STAT5A/P-STAT5 signaling in breast cancer.Journal of Cancer · 2022Article
- Endothelial cell-derived extracellular vesicles impair the angiogenic response of coronary artery endothelial cells.Frontiers in cardiovascular medicine · 2022Article
- Effect of Extracellular Vesicles From Multiple Cells on Vascular Smooth Muscle Cells in Atherosclerosis.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Soluble factors and cell-derived extracellular vesicles (EVs) control vascular cell fate during inflammation. The present study investigates the impact of Interleukin 3 (IL-3) on EV release by endothelial cells (ECs), the mechanisms involved in EV release and paracrine actions. We found that IL-3 increases EV release, which is prevented by IL-3Ralpha blockade. EVs released upon IL-3 stimulation were able to induce pro-angiogenic signals as shown by chromatin immunoprecipitation (ChIP) assay performed on the promoter region of cyclin D1 and tridimensional tube-like structure formation. We herein demonstrate that these effects rely on the transfer of miR-126-3p, pre-miR-126 and, more importantly, of activated signal transduction and activator of transcription 5 (pSTAT5) from IL-3-EV cargo into recipient ECs. We show, using the dominant negative form (ΔN)STAT5 and an activated STAT5 (1*6STAT5) constructs, that STAT5 drives IL-3-mediated EV release, miR-126-3p and pSTAT5 content. Finally, using EVs recovered from ΔNSTAT5 expressing ECs, we provide evidence that miR-126-3p and pSTAT5 trafficking is relevant for IL-3-mediated paracrine pro-angiogenic signals. These results indicate that IL-3 regulates EC-EV release, cargo and IL-3 angiogenic paracrine action via STAT5. Moreover, these results provide evidence that EC-derived IL-3-EVs can serve as pro-angiogenic clinical delivery wound healing devices.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.