Endothelial Repair in Childhood Arterial Ischaemic Stroke with Cerebral Arteriopathy

Eleftheriou, Despina; Ganesan, Vijeya; Hong, Ying; Klein, Nigel; Brogan, Paul A.

doi:10.1159/000381963

Cited by 17 publications

(13 citation statements)

References 12 publications

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“…Hong et al observed, however, that the function of these elevated circulating EPCs was impaired in children with active vasculitis [ 47 ]. Similar findings were observed by Eleftheriou et al in children with arterial stroke caused by cerebral vasculitis [ 67 ].…”

Section: Other Biomarkers and Miscellaneous Vasculitides: Endothelialsupporting

confidence: 91%

Vasculitis update: pathogenesis and biomarkers

Brogan

Eleftheriou

2017

Pediatr Nephrol

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Better understanding of the pathogenesis and treatment of primary systemic vasculitides (PSV) has led to the development of many potentially clinically relevant biomarkers. Genome-wide association studies have highlighted that MHC class II polymorphisms may influence the development of particular anti-neutrophil cytoplasmic antibody (ANCA) serotypes, but not the clinical phenotype of ANCA-associated vasculitis (AAV). Although ANCAs are overall poor biomarkers of disease activity, they may be useful for the prediction of flares of renal and/or pulmonary vasculitis. Moreover, patients with proteinase 3 (PR3)-AAV may respond better to rituximab than cyclophosphamide. Newer biomarkers of renal vasculitis in AAV include urinary soluble CD163, and may in the future reduce the requirement for renal biopsy. Better understanding of dysregulated neutrophil activation in AAV has led to the identification of novel biomarkers including circulating microparticles, and neutrophil extracellular traps (NETs), although their clinical utility has not yet been realised. Studies examining endothelial injury and repair responses have additionally revealed indices that may have utility as disease activity and/or prognostic biomarkers. Last, next-generation sequencing technologies are revealing monogenic forms of vasculitis, such as deficiency of adenosine deaminase type 2 (DADA2), and are profoundly influencing the approach to the diagnosis and treatment of vasculitis in the young.

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Section: Other Biomarkers and Miscellaneous Vasculitides: Endothelialsupporting

confidence: 91%

Vasculitis update: pathogenesis and biomarkers

Brogan

Eleftheriou

2017

Pediatr Nephrol

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“…With the ability of differentiation and proliferation, EPCs are in a dormant state in the bone marrow under normal circumstances. Being stimulated by tissue ischemia, trauma, and other stimuli, EPCs can passively enter the peripheral blood circulation, reach the damage site of ischemic tissue, and form endothelial cells there through differentiation and proliferation to involve in endothelial repair and angiogenesis [11–13]. Particularly, EPCs has been thought to play a major role in pathophysiology of ischemic cerebral diseases [14].…”

Section: Introductionmentioning

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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“…7,9,17,18 Classical determinants for stroke and biomarkers reflecting endothelial injury and repair can also predict outcome. 17,19,20,21 There is also a trend for a better outcome 6 and few recurrences 17 in children treated with aspirin. In our former report of TCA, recurrence occurred in 3 of 4 children without treatment versus only one of 11 who received aspirin.…”

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confidence: 99%