Endothelial progenitor cells in acute ischemic stroke

Martí‐Fàbregas, Joan; Crespo, Javier; Delgado‐Mederos, Raquel; Martínez-Ramírez, Sergi; Peña, Esther; Marín, Rebeca; Dinia, Lavinia; Jiménez‐Xarrié, Elena; Fernández-Arcos, Ana; Pérez‐Pérez, Jesús; Querol, Luís; Suárez‐Calvet, Marc; Badimon, Lina

doi:10.1002/brb3.175

Cited by 37 publications

(30 citation statements)

References 40 publications

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“…MiR‐146a in early EPCs could promote vascular repair by suppressing inflammation during cardiovascular injury; while miR‐126 in late EPCs, directly promotes angiogenesis and vascular repair [28]. However, another study shows after acute ischemic stroke, the release of cytokines and trophic factors may contribute to an increased EPC production and mobilization [29].…”

Section: Discussionmentioning

confidence: 99%

Regulatory effects of miR‐146a/b on the function of endothelial progenitor cells in acute ischemic stroke in mice

Sun

Zhang

et al. 2017

The Kaohsiung J of Med Scie

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The study aims to explore how microRNA-146a/b (miR-146a/b) regulates the function of endothelial progenitor cells (EPCs) in acute ischemic stroke in mice. Eighty male SPF C57BL/6J mice were evenly divided into the model-6 h, model-12 h, model-24 h (mice suffered from middle cerebral artery occlusion [MCAO] for 6 h, 12 h and model-24 h) and normal groups. EPCs were transfected and assigned into the control, MCAO, MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. The qRT-PCR was used to detect miR-146a/b expression in EPCs. Expressions of tumor necrosis factor receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK1) were detected using western blotting. Cell proliferation and migration of EPCs were testified using CCK-8 assay and scratch test, respectively. Angiogenesis ability of EPCs was observed under microscope. MiR-146a and miR-146b expressions were lower in the model groups than the normal group. There were up-regulated TRAF6 and IRAK1 expressions in the model-6 h, model-12 h and model-24 h groups compared with the normal group. And there were down-regulated TRAF6 and IRAK1 expressions in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups than in the MCAO group. Compared with the control group, the proliferation, migration and angiogenesis ability of EPCs were significantly lower in the MCAO group, but higher in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. Besides, the miR-146a/b group showed more enhancement than the MCAO-miR-146a and MCAO-miR-146b groups. MiR-146a/b could down-regulate the TRAF6 and IRAK1 expressions and promote proliferation, migration and angiogenesis ability of EPCs, which was important for recovery of patients with hyperacute ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Regulatory effects of miR‐146a/b on the function of endothelial progenitor cells in acute ischemic stroke in mice

Sun

Zhang

et al. 2017

The Kaohsiung J of Med Scie

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“…Exclusion criteria were: (1) A previous modified Rankin scale (RS) score higher than 2; (2) A NIHSS score of 0; (3) The lack of processing of the blood sample within 30 minutes after extraction, as this was the pre-defined time window to obtain reliable results. We evaluated the same patients in a previous study[ 10 ] in which we searched for markers of EPC counts and for the association between EPC counts and short-term prognosis in the acute stage of ischemic stroke.…”

Section: Methodsmentioning

confidence: 99%

Circulating Endothelial Progenitor Cells and the Risk of Vascular Events after Ischemic Stroke

et al. 2015

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Background and PurposeWe evaluated the hypothesis that the number of circulating EPC could be associated with the risk of stroke recurrence (SR) or vascular events (VE) after an ischemic stroke.MethodsWe studied prospectively consecutive patients with cerebral infarction within the first 48 hours after the onset. We recorded demographic factors, vascular risk factors, previous Rankin scale (RS) score, and etiology. We analyzed EPC counts by flow cytometry in blood collected at day 7 and defined EPC as CD34+/CD133+/KDR+ cells. Mean follow-up was 29.3 ± 16 months. We evaluated SR as well as VE. Patients were classified as to the presence or absence of EPC in the circulation (either EPC+ or EPC-). Bivariate analyses, Kaplan-Meier survival curves and Cox regression models were used.ResultsWe included 121 patients (mean age 70.1±12.6 years; 65% were men). The percentage of EPC+ patients was 47.1%. SR occurred in 12 (9.9%) and VE in 18 (14.9%) patients. SR was associated significantly with a worse prior RS score, previous stroke and etiology, but not with EPC count. VE were associated significantly with EPC-, worse prior RS score, previous stroke, high age, peripheral artery disease and etiology. Cox regression model showed that EPC- (HR 7.07, p=0.003), age (HR 1.08, p=0.004) and a worse prior RS score (HR 5.8, p=0.004) were associated significantly with an increased risk of VE.ConclusionsThe absence of circulating EPC is not associated with the risk of stroke recurrence, but is associated with an increased risk of future vascular events.

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“…Transplanted EPCs are able to incorporate into vessels around areas of infarction through neovascularization 306 . Studies on patients suffering from strokes have revealed that an increase in EPC concentration in the circulation is a positive sign for better outcomes of recovery 302,303,307 , while failure to elevate blood EPCs often implies a poorer prognosis 301,308 . In animal models of brain ischemia, systemic or intra-carotid arterial administration of EPCs has been shown to enhance neovascularization and neurogenesis, reduce the severity of brain injuries, and improve long-term neurobehavioral outcomes 309–311 .…”

Section: Application Of Vascular Precursor Cells In the Treatment Of mentioning

confidence: 99%

Vascular precursor cells in tissue injury repair

Shi

Zhang

Yin

et al. 2017

Translational Research

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Vascular precursor cells include stem and progenitor cells giving rise to all mature cell types in the wall of blood vessels. Upon tissue injury, local hypoxia and inflammation result in generation of vasculogenic mediators which orchestrate migration of vascular precursor cells from their niche environment to the site of tissue injury. The intricate crosstalk among signaling pathways coordinates vascular precursor cell proliferation and differentiation during neovascularization. Establishment of normal blood perfusion plays an essential role in effective repair of the injured tissue. In recent years, studies on molecular mechanisms underlying the regulation of vascular precursor cell function have achieved substantial progress, which promotes exploration of vascular precursor cell-based approaches to treat chronic wounds and ischemic diseases in vital organ systems. Verification of safety and establishment of specific guidelines for the clinical application of vascular precursor cell-based therapy remain major challenges in the field.

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Endothelial progenitor cells in acute ischemic stroke

Cited by 37 publications

References 40 publications

Regulatory effects of miR‐146a/b on the function of endothelial progenitor cells in acute ischemic stroke in mice

Regulatory effects of miR‐146a/b on the function of endothelial progenitor cells in acute ischemic stroke in mice

Circulating Endothelial Progenitor Cells and the Risk of Vascular Events after Ischemic Stroke

Vascular precursor cells in tissue injury repair

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