ArticleScientific reports2016
XBP1 splicing triggers miR-150 transfer from smooth muscle cells to endothelial cells via extracellular vesicles.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- An Inhibitory Aptamer Against PDGF-C Overcomes Anti-VEGF Refractoriness and Reduces Choroidal Neovascularization and Fibrosis.Investigative ophthalmology & visual science · 2026Article
- Diversity of extracellular vesicle sources in atherosclerosis: role and therapeutic application.Angiogenesis · 2025Review
- ERS regulates endometrial epithelial cell autophagy through XBP1s-mediated activation of the PI3K/AKT pathway.Scientific reports · 2025Article
- Emerging Strategies for Revascularization: Use of Cell-Derived Extracellular Vesicles and Artificial Nanovesicles in Critical Limb Ischemia.Bioengineering (Basel, Switzerland) · 2025Review
- Emerging role of sphingolipids and extracellular vesicles in development and therapeutics of cardiovascular diseases.International journal of cardiology. Heart & vasculature · 2024Review
- Basic Pathogenic Mechanisms and Epigenetic Players Promoted by Extracellular Vesicles in Vascular Damage.International journal of molecular sciences · 2023Review
- Extracellular vesicles as biomarkers and modulators of atherosclerosis pathogenesis.Frontiers in cardiovascular medicine · 2023Review
- Extracellular Vesicles and Vascular Inflammation.Advances in experimental medicine and biology · 2023Article
- Bioengineering Extracellular Vesicles for the Treatment of Cardiovascular Diseases.Advanced biology · 2022Review
- Article
- Exosomes in cardiovascular diseases: a blessing or a sin for the mankind.Molecular and cellular biochemistry · 2022Review
- The Function of KDEL Receptors as UPR Genes in Disease.International journal of molecular sciences · 2021Review
- A narrative review of exosomes in vascular calcification.Annals of translational medicine · 2021Review
- Cardiovascular Exosomes and MicroRNAs in Cardiovascular Physiology and Pathophysiology.Journal of cardiovascular translational research · 2021Review
- Mechanisms of Action of MiRNAs and LncRNAs in Extracellular Vesicle in Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- Extracellular vesicles-derived miR-150-5p secreted by adipose-derived mesenchymal stem cells inhibits CXCL1 expression to attenuate hepatic fibrosis.Journal of cellular and molecular medicine · 2021Article
- Extracellular vesicle signalling in atherosclerosis.Cellular signalling · 2020Review
- Proteostasis and Beyond: ATF6 in Ischemic Disease.Trends in molecular medicine · 2019Review
- The Exosome-Derived Biomarker in Atherosclerosis and Its Clinical Application.Journal of cardiovascular translational research · 2019Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The interaction between endothelial cells (ECs) and smooth muscle cells (SMCs) plays a critical role in the maintenance of vessel wall homeostasis. The X-box binding protein 1 (XBP1) plays an important role in EC and SMC cellular functions. However, whether XBP1 is involved in EC-SMC interaction remains unclear. In this study, In vivo experiments with hindlimb ischemia models revealed that XBP1 deficiency in SMCs significantly attenuated angiogenesis in ischemic tissues, therefore retarded the foot blood perfusion recovery. In vitro studies indicated that either overexpression of the spliced XBP1 or treatment with platelet derived growth factor-BB up-regulated miR-150 expression and secretion via extracellular vesicles (EVs). The XBP1 splicing-mediated up-regulation of miR-150 might be due to increased stability. The SMC-derived EVs could trigger EC migration, which was abolished by miR-150 knockdown in SMCs, suggesting miR-150 is responsible for SMC-stimulated EC migration. The SMC-derived miR-150-containing EVs or premiR-150 transfection increased vascular endothelial growth factor (VEGF)-A mRNA and secretion in ECs. Both inhibitors SU5416 and LY294002 attenuated EVs-induced EC migration. This study demonstrates that XBP1 splicing in SMCs can control EC migration via SMC derived EVs-mediated miR-150 transfer and miR-150-driven VEGF-A/VEGFR/PI3K/Akt pathway activation, thereby modulating the maintenance of vessel wall homeostasis.
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Registered trials
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.