MiRNA-27b Regulates Angiogenesis by Targeting AMPK in Mouse Ischemic Stroke Model

Yuan, Yimei; Zhang, Zhaoguang; Wang, ZhenGang; Liu, Jinlan

doi:10.1016/j.neuroscience.2018.11.041

Cited by 34 publications

(26 citation statements)

References 46 publications

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“…Increasing evidence suggests that miRNAs are involved in the process of ischemic stroke (Zhang et al, 2017). A large number of studies have used miRNA treatment to reduce ischemic brain injury and functional recovery after stroke (Volný et al, 2015;Sen, 2019;Van Kralingen et al, 2019;Yuan et al, 2019). Based on this fact, we explored the effect of exosomal miR-146b on neural stem cell differentiation after ischemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Electro-Acupuncture Promotes the Differentiation of Endogenous Neural Stem Cells via Exosomal microRNA 146b After Ischemic Stroke

Zhang

Jin

Wang

et al. 2020

Front. Cell. Neurosci.

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Background: Evidences indicate that exosomes-mediated delivery of microRNAs (miRNAs or miRs) is involved in the neurogenesis of stroke. This study was to investigate the role of exosomal miRNAs in non-drug therapy of electro-acupuncture (EA) regulating endogenous neural stem cells for stroke recovery. Methods: The model of focal cerebral ischemia and reperfusion in rats were established by middle cerebral artery occlusion (MCAO) and treated by EA. The exosomes were extracted from peri-ischemic striatum and identified by exosomal biomarkers, and detected differentially expressed miRNAs with microarray chip. Primary stem cells were cultured, and oxygen-glucose deprivation and reperfusion (OGD/R) was used to mimic vitro ischemic injury. Results: The levels of exosomal biomarkers TSG101 and CD81 were increased in peri-ischemic striatum after EA treatment, and we revealed 25 differentially expressed miRNAs in isolated exosomes, of which miR-146b was selected for further analysis, and demonstrated that EA increased miR-146b expression and its inhibitors could block the effects. Subsequently, we confirmed that EA upregulated miR-146b expression to promote neural stem cells differentiation into neurons in peri-ischemic striatum. In vitro, it was verified that OGD/R hindered neural stem cells differentiation, and miR-146b inhibitors furtherly suppressed its differentiation, simultaneously NeuroD1 was involved in neural stem cells differentiation into neurons. Moreover, in vivo we found EA promoted NeuroD1-mediated neural stem cells differentiation via miR-146b. In addition, EA also could improve neurological deficits through miR-146b after ischemic stroke. Conclusion: EA promotes the differentiation of endogenous neural stem cells via exosomal miR-146b to improve neurological injury after ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Electro-Acupuncture Promotes the Differentiation of Endogenous Neural Stem Cells via Exosomal microRNA 146b After Ischemic Stroke

Zhang

Jin

Wang

et al. 2020

Front. Cell. Neurosci.

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“…ese results therefore plainly indicate that the miR-27b-ACOT2 axis promotes lipid accumulation and adipocyte di erentiation, process which result in NAFLD pathogenesis. Several studies have shown that miR-27b regulates not only adipogenesis, but also cell proliferation, angiogenesis, and tumor development [14,15,40,41]. Nonetheless, the role of miR-27b has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, several studies have shown that PPARγ activation can prevent the progression of hepatic steatosis in murine models [46], and that treatment with the PPARγ agonist rosiglitazone exerts similar e ects [47]. e protective e ects of PPARγ could be the result of higher insulin protein kinase, which induced angiogenic tube formation and the migration of endothelial cells [15]. In addition, miR-27b highly expressed in sheep skeletal muscle directly reduced myostatin mRNA and led to cell proliferation [41].…”

Section: Discussionmentioning

confidence: 99%

“…Among altered miRNAs in patients, we found that miR-27b is remarkedly increased in liver tissue and serum from the early phase of NAFLD to severe NASH [12,13]. It has been reported that miR-27b is involved in cell proliferation, differentiation, migration, invasion, metastasis, multi-drug resistance in various tumor cells [14][15][16][17][18]. However, the exact role of miR-27b in NAFLD pathogenesis, and in particular its relationship to adipocyte differentiation, remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Up-Regulated MicroRNA-27b Promotes Adipocyte Differentiation via Induction of Acyl-CoA Thioesterase 2 Expression

Murata

Yamashiro

Kessoku

et al. 2019

BioMed Research International

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Nonalcoholic fatty liver disease (NAFLD) is characterized by a spectrum of liver pathologies, from simple steatosis to steatohepatitis. Recent studies have increasingly noted the aberrant expression of microRNAs closely related to NAFLD pathologies. We have previously shown the presence of increased levels of microRNA-27b (miR-27b) in patients with NAFLD. In this study, we investigated the role of miR-27b in NAFLD by examining the impact of up-regulated miR-27b on the differentiation of preadipocytes into mature adipocytes. We found that miR-27b-3p remarkably enhances the adipocyte differentiation of 3T3-L1 cells associated with lipid accumulation and intracellular triglyceride contents. Furthermore, we have demonstrated not only that miR-27b-3p induces acyl-CoA thioesterase 2 (ACOT2) expression in 3T3-L1 cells, but also that the knockdown of ACOT2 suppresses lipid accumulation and adipocyte differentiation in both the presence and absence of miR-27b-3p treatment. Our data strongly suggest that the miR-27b-ACOT2 axis is an important pathway in adipocyte differentiation and may play a role in the pathogenesis of NAFLD.

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“…Since efficient angiogenesis can accelerate recovery after stroke, specific angiogenic miRNAs could be a potent therapeutic target. Yuan, Zhang, Wang, and Liu (2019) demonstrated that injection of lentivirus miR‐27b inhibitor (anti‐miR‐27b‐5p) led to the enhancement of angiogenesis in a middle cerebral artery occlusion (MCAO) mice model via stimulation of AMPK and improved cognitive performance. Considering the regulatory role of the miR‐15a/16‐1 cluster in the angiogenesis, endothelial cell‐selective miR‐15a/16‐1 conditional KO (EC‐miR‐15a/16‐1 cKO) in mice proceeded cerebral angiogenesis following MCAO via enhancement of Src signaling pathway.…”

Section: Neurological Disorders Associated With Cognitive Impairmentmentioning

confidence: 99%

MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models

Bahlakeh

Gorji

Soltani

et al. 2020

Journal Cellular Physiology

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Cognitive dysfunction is a state of losing or having difficulties in remembering, learning, focusing, or making decisions that impact individual healthy life. Small single-stranded and nonprotein coding RNAs, microRNAs (miRNAs) participate actively in regulatory processes, incorporate cognitive signaling pathways, and intensely affect cognitive evolution. miRNAs exert their modification activities through translational or transcriptional processes. Reportedly, cognitive impairment and dementia are rising, especially in developing countries. Herein we provided a brief review of original studies addressing miRNA changes in the most common neurological diseases with a focus on dementia and Alzheimer's disease. It must be How to cite this article: Bahlakeh G, Gorji A, Soltani H, Ghadiri T. MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models.

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MiRNA-27b Regulates Angiogenesis by Targeting AMPK in Mouse Ischemic Stroke Model

Cited by 34 publications

References 46 publications

Electro-Acupuncture Promotes the Differentiation of Endogenous Neural Stem Cells via Exosomal microRNA 146b After Ischemic Stroke

Electro-Acupuncture Promotes the Differentiation of Endogenous Neural Stem Cells via Exosomal microRNA 146b After Ischemic Stroke

Up-Regulated MicroRNA-27b Promotes Adipocyte Differentiation via Induction of Acyl-CoA Thioesterase 2 Expression

MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models

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