Increasing the expression of microRNA-126-5p in the temporal muscle can promote angiogenesis in the chronically ischemic brains of rats subjected to two-vessel occlusion plus encephalo-myo-synangiosis

Chen, Chuan; Ling, Cong; Gong, Jianbin; Li, Chao; Zhang, Liying; Gao, Shuang-Qi; Li, Zhangyu; Huang, Tengchao; Wang, Hui; Guo, Ying

doi:10.18632/aging.103431

Cited by 16 publications

(14 citation statements)

References 32 publications

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“…36 Two-vessel occlusion adaptations, such as staged ligation, have been described to counter these issues. 15,37 While a grossly similar reduction in CBF (average of 24.18% of baseline) has been observed, this modification affords a more progressive decline that may mitigate acute deficit. Unilateral occlusion of the CCA has also been described.…”

Section: Carotid Artery Occlusion or Stenosismentioning

confidence: 70%

“…Surgical models utilize mechanical occlusion or narrowing of extracranial and/ or intracranial vasculature to replicate stenosis and accompanying cerebral ischemia. 15,16 Immunological models attempt to induce a "vasculitic" syndrome to reproduce the morphological changes observed in the intracranial vasculature of patients with MMD. 17,18 Finally, with the identification of the RNF213 susceptibility gene, various knockout, knock-in, or knockdown genetic models have been generated to study its impact on vasculogenesis, angiogenesis, and remodeling.…”

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confidence: 99%

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Experimental animal models for moyamoya disease and treatment: a pathogenesis-oriented scoping review

Rallo

Akel

Gurram

et al. 2021

Neurosurgical Focus

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OBJECTIVE Moyamoya disease (MMD) is an intracranial steno-occlusive pathology characterized by progressive narrowing of proximal large vessels, including the terminal internal carotid arteries (ICAs), middle cerebral arteries, or anterior cerebral arteries. Named for the “puff of smoke” appearance of the anomalous vascularization visualized on cerebral angiography, MMD lacks a well-defined etiology, although significant insights have been made, including the identification of a susceptibility gene, RNF213, in humans with the disease. A limitation to advancing the understanding and treatment of MMD has been the lack of experimental animal models that authentically reflect the clinical pathogenesis. In an effort to analyze characteristics of currently available models and identify strategies for future model generation, the authors performed a scoping review of experimental animal models that have been used to study MMD. METHODS A systematic search of PubMed, Web of Science, and Scopus was performed to identify articles describing animal models used to study MMD. Additional articles were identified via citation searching. Study selection and data extraction were performed by two independent reviewers based on defined inclusion and exclusion criteria. RESULTS A total of 44 articles were included for full-text review. The methods used to generate these animal models were broadly classified as surgical (n = 25, 56.8%), immunological (n = 7, 15.9%), genetic (n = 6, 13.6%), or a combination (n = 6, 13.6%). Surgical models typically involved permanent ligation of one or both of the common carotid arteries or ICAs to produce chronic cerebral hypoperfusion. Genetic models utilized known MMD or cerebrovascular disease-related genes, such as RNF213 or ACTA2, to induce heritable cerebral vasculopathy. Finally, immunological models attempted to induce vasculitis-type pathology by recapitulating the inflammatory milieu thought to underlie MMD. CONCLUSIONS Models generated for MMD have involved three general approaches: surgical, immunological, and genetic. Although each reflects a key aspect of MMD pathogenesis, the failure of any individual model to recapitulate the development, progression, and consequences of the disease underscores the importance of future work in developing a multietiology model.

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Section: Carotid Artery Occlusion or Stenosismentioning

confidence: 70%

mentioning

confidence: 99%

Experimental animal models for moyamoya disease and treatment: a pathogenesis-oriented scoping review

Rallo

Akel

Gurram

et al. 2021

Neurosurgical Focus

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“…As previously described ( 25 ), 30 μg protein samples were separated by 10% SDS-PAGE gel, and then transferred to polyvinylidene fluoride (PVDF, pore size, 0.45 um) membranes (Millipore Billerica, USA). The membranes were blocked with 5% non-fat dry milk for 1 h, followed by incubation overnight at 4°C with the following primary antibodies: rabbit anti-SH3RF2 (1:1,000), rabbit anti-HMGB1 (1:1,000), mice anti-EGFP (1:1,000, mice anti-GAPDH (1:1,000), and mice anti-β-actin (1:1,000).…”

Section: Methodsmentioning

confidence: 99%

Nonoxid-HMGB1 Attenuates Cognitive Impairment After Traumatic Brain Injury in Rats

et al. 2022

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Traumatic brain injury (TBI) is a major global burden of health. As an accepted inflammatory mediator, high mobility group box 1 (HMGB1) is found to be effective in facilitating neurogenesis and axonal regeneration. SH3RF2 (also known as POSHER), an E3 ligase SH3 domain-containing ring finger 2, belongs to the SH3RF family of proteins. Here, we aimed to investigate the role of redox states of HMGB1 on neurite outgrowth and regeneration both in vitro and in vivo. In this study, distinct recombinant HMGB1 redox isoforms were used. Sequencing for RNA-seq and data analysis were performed to find the potential downstream target of nonoxid-HMGB1 (3S-HMGB1). Protein changes and distribution of SH3RF2 were evaluated by western blot assays and immunofluorescence. Lentivirus and adeno-associated virus were used to regulate the expression of genes. Nonoxid-HMGB1-enriched exosomes were constructed and used to treat TBI rats. Neurological function was evaluated by OF test and NOR test. Results demonstrated that nonoxid-HMGB1 and fr-HMGB1, but not ds-HMGB1, promoted neurite outgrowth and axon elongation. RNA-seq and western blot assay indicated a significant increase of SH3RF2 in neurons after treated with nonoxid-HMGB1 or fr-HMGB1. Notably, the beneficial effects of nonoxid-HMGB1 were attenuated by downregulation of SH3RF2. Furthermore, nonoxid-HMGB1 ameliorated cognitive impairment in rats post-TBI via SH3RF2. Altogether, our experimental results suggest that one of the promoting neurite outgrowth and regeneration mechanisms of nonoxid-HMGB1 is mediated through the upregulated expression of SH3RF2. Nonoxid-HMGB1 is an attractive therapeutic candidate for the treatment of TBI.

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“…Fang et al demonstrated that miR‐29b suppresses tumor angiogenesis, invasion, and metastasis by regulating matrix metalloproteinase 2 expression 20 . Chen et al demonstrated that increasing miR‐126‐5p expression in the temporal muscle can promote endothelial cell proliferation and angiogenesis in chronically ischemic brains of two‐vessel occlusion plus EMS rats through the PI3K/Akt pathway 21 …”

Section: Introductionmentioning

confidence: 99%

“… 20 Chen et al demonstrated that increasing miR‐126‐5p expression in the temporal muscle can promote endothelial cell proliferation and angiogenesis in chronically ischemic brains of two‐vessel occlusion plus EMS rats through the PI3K/Akt pathway. 21 …”

Section: Introductionmentioning

confidence: 99%

Use of a panel of four microRNAs in CSF as a predicted biomarker for postoperative neoangiogenesis in moyamoya disease

et al. 2021

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Introduction and Aims At present, the treatment for moyamoya disease (MMD) primarily consists of combined direct and indirect bypass surgery. Nevertheless, more than half of indirect bypass surgeries fail to develop good collaterals from the dura and temporal muscle. This study aimed to investigate whether microRNAs (miRNAs) in cerebrospinal fluid (CSF) could serve as biomarkers for the prediction of postoperative collateral formation. Methods Moyamoya disease patients with indirect bypass surgery were divided into angiogenesis and non‐angiogenesis groups, CSF was obtained, and miRNA sequencing was performed using the CSF. Candidate miRNAs were filtered and subsequently verified through qRT‐PCR. The diagnostic utility of these differential miRNAs was investigated by using receiver operating characteristic (ROC) curve analysis. Finally, the potential biological processes and signaling pathways associated with candidate miRNAs were analyzed using R software. Results The expression levels of four miRNAs (miR‐92a‐3p, miR‐486‐3p, miR‐25‐3p, and miR‐155‐5p) were significantly increased in the angiogenesis group. By combining these four miRNAs (area under the curve [AUC] =0.970), we established an accurate predictive model of collateral circulation after indirect bypass surgery in MMD patients. GO and KEGG analyses demonstrated a high correlation with biological processes and signaling pathways related to angiogenesis. Conclusion The 4‐miRNA signature is a good model to predict angiogenesis after indirect bypass surgery and help the surgeon to select a appreciate bypass strategy.

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Increasing the expression of microRNA-126-5p in the temporal muscle can promote angiogenesis in the chronically ischemic brains of rats subjected to two-vessel occlusion plus encephalo-myo-synangiosis

Cited by 16 publications

References 32 publications

Experimental animal models for moyamoya disease and treatment: a pathogenesis-oriented scoping review

Experimental animal models for moyamoya disease and treatment: a pathogenesis-oriented scoping review

Nonoxid-HMGB1 Attenuates Cognitive Impairment After Traumatic Brain Injury in Rats

Use of a panel of four microRNAs in CSF as a predicted biomarker for postoperative neoangiogenesis in moyamoya disease

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