Browsing by Subject "Endothelial progenitor cells"

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    Baicalin promotes migration and angiogenesis of endothelial progenitor cells but impedes thrombus formation via SIRT1/NF-κB signaling in a rat model of deep vein thrombosis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Xie, Jinfeng; Liao, Yonggui; Wang, Dile
    Background. Deep vein thrombosis (DVT) is the third most prevalent vascular disease worldwide, seriously threatening human health. Baicalin, a flavonoid isolated from the roots of Scutellaria baicalensis, has been identified to play a crucial role in various vascular diseases. The study aimed to explore the efficacy and underlying mechanisms of baicalin in DVT. Methods. Endothelial progenitor cells (EPCs) were differentiated from peripheral blood mononuclear cells isolated from rat bone marrow. Dil-ac-LDL/FITC-UEA-1 double staining and flow cytometry analysis were conducted for the identification of EPCs. The angiogenesis and migration of EPCs in vitro were tested by a tube formation assay and Transwell assay, respectively. DVT rat models were established by stenosis of the inferior vena cava (IVC). After the euthanasia of rats, thrombi in the IVC were collected and weighed, and histological alterations in IVC tissue were measured by H&E staining. The protein levels of SIRT1, p-P65, and p65 in rat IVC tissues were quantified via western blotting. Results. EPCs used in this study displayed a spindle-like shape and were positive for endothelial cell-specific markers, suggesting the phenotypic characteristics of EPCs. Baicalin enhanced the migratory and angiogenetic abilities of EPCs in vitro. For in vivo experiments, baicalin reduced thrombus weight and mitigated DVT formation in model rats. Moreover, baicalin activated SIRT but repressed NF-κB signaling in IVC tissues of DVT rats. Conclusion. Baicalin facilitates migration and angiogenesis of EPCs but impedes thrombus formation via regulation of SIRT1/NF-κB signaling in DVT model rats.
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    Exosomes derived from endothelial progenitor cells ameliorate glyoxylate deprivation (OGD)-induced neuronal apoptosis by delivering miR-221-3p
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2023) Pan, Jie; Wu, Tingting; Chen, Bo; Wu, Huadong
    This study evaluated the potential of endothelial progenitor cell (EPC)-derived exosomes as a therapeutic factor for neuronal apoptosis. Mouse EPCs were cultured in vitro, and exosomes were isolated and identified using transmission electron microscopy (TEM), particle size analysis and by determining the protein expressions of exosome markers (CD9, CD63 and Alix). The apoptotic rate of OGD-treated neurons was detected by Flow cytometry assay. The mRNA and protein expression levels were detected by RT-PCR and Western blot assay, respectively. Luciferase reporter assays determined the interaction between miR-221-3p and Bcl2l11. The results showed that most exosomes are 80-120 nm in diameter. Western blot assay showed that CD9, CD63 and Alix were enriched in exosomes. EPCderived exosomes ameliorated OGD-induced neuronal apoptosis. Mechanistically, miR-221-3p from EPCderived exosomes decreased the expression of bcl2l11 in OGD-induced neuronal apoptosis. Moreover, exosomes from miR-221-3p mimics transfected EPCs reduced OGD-induced neuronal apoptosis. In conclusion, miR221-3p in EPC derived exosomes ameliorates OGDinduced neuronal apoptosis, which establish its potential as a new therapeutic method for patients with cerebrovascular diseases.
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    Proangiogenic hematopoietic cells of monocytic origin: roles in vascular regeneration and pathogenic processes of systemic sclerosis
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2013) Yamaguchi, Yukie; Kuwana, Masataka
    New blood vessel formation is critical, not only for organ development and tissue regeneration, but also for various pathologic processes, such as tumor development and vasculopathy. The maintenance of the postnatal vascular system requires constant remodeling, which occurs through angiogenesis, vasculogenesis, and arteriogenesis. Vasculogenesis is mediated by the de novo differentiation of mature endothelial cells from endothelial progenitor cells (EPCs). Early studies provided evidence that bone marrow-derived CD14+ monocytes can serve as a subset of EPCs because of their expression of endothelial markers and ability to promote neovascularization in vitro and in vivo. However, the current consensus is that monocytic cells do not give rise to endothelial cells in vivo, but function as support cells, by promoting vascular formation and repair through their immediate recruitment to the site of vascular injury, secretion of proangiogenic factors, and differentiation into mural cells. These monocytes that function in a supporting role in vascular repair are now termed monocytic pro-angiogenic hematopoietic cells (PHCs). Systemic sclerosis (SSc) is a multisystem connective tissue disease characterized by excessive fibrosis and microvasculopathy, along with poor vascular formation and repair. We recently showed that in patients with SSc, circulating monocytic PHCs increase dramatically and have enhanced angiogenic potency. These effects may be induced in response to defective vascular repair machinery. Since CD14+ monocytes can also differentiate into fibroblast-like cells that produce extracellular matrix proteins, here we propose a new hypothesis that aberrant monocytic PHCs, once mobilized into circulation, may also contribute to the fibrotic process of SSc.