Inhibition of miR-34a ameliorates cerebral ischemia/reperfusion injury by targeting brain-derived neurotrophic factor

Zhu, Shilin; Tang, Jianghong; Lan, Lan; Su, Feng

doi:10.5114/aoms/143303

Cited by 2 publications

(2 citation statements)

References 30 publications

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“…Moreover, the model that we used in our study, also have limitations regarding stroke attack stability, predictability, infarct sizes, and locations, complicating the translation of findings to clinical applications. The study was also unable to identify some recently explored aspects of molecular insight of ischemia, such as involvement of miRNAs, which is also an active area of ischemia research [41,42].…”

Section: P R E P R I N Tmentioning

confidence: 93%

Single Cell sequencing reveals heterogenicity of differential gene-expression and altered interactome in post ischemic mice brain cells

Lu,

Hou,

Wang

et al. 2024

Arch Med Sci

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IntroductionIschemia, resulting from reduced blood supply due to arterial constriction or blockages, leads to oxygen and nutrient deprivation, impacting various body systems and contributing to numerous diseases. Despite extensive research on ischemia, molecular studies with spatial and temporal specificity are limited. Our study utilized single-cell genomics to investigate hypoxia-induced changes in the mouse brain at 30 and 60 minutes of exposure, aiming to map cellular trajectories, ontologies, and expression patterns in a cell-specific manner.Material and methodsWe developed a mouse model of hypoxia using the thread-plug method. Experimental groups were exposed to hypoxia for 30 minutes (T_30) and 60 minutes (T_60), with a sham surgery group as control. After excising the cerebral cortex, we performed nuclear isolation and library construction for spatio-temporal analysis of cortical cells. Data analysis included differential gene expression, trajectory analysis, examination of gene regulatory networks, and hallmark analysis.ResultsSingle-cell genomics analysis revealed 12 distinct cell populations with different transcriptomic profiles. Spatio-temporal distinctions in cell signaling were observed, showing a switch from Ras GTPase signaling to calmodulin and calcium-dependent signaling between the two hypoxia levels. In the T_30 group, distal axons and growth cones were transcriptionally active, while in the T_60 group, cell edges and post-synaptic areas were more active. The synaptic vesicle cycle was implicated in transcriptional changes across the T_30 and T_60 groups.ConclusionsOur single-cell genomics study provides new insights into cellular dynamics during hypoxia. The identified cell populations and molecular pathways highlight potential targets for further research and the development of targeted therapies for ischemia.

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Section: P R E P R I N Tmentioning

confidence: 93%

Single Cell sequencing reveals heterogenicity of differential gene-expression and altered interactome in post ischemic mice brain cells

Lu,

Hou,

Wang

et al. 2024

Arch Med Sci

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“…Antagonism of miR-34a using gentamycin in an established in vitro stroke cell line showed increased cell viability and protected cells against oxidative damage ( Izadi et al, 2023 ). Increased miR-34a has also been correlated with a decrease in brain derived neurotrophic factor (BDNF) ( Zhu et al, 2021 ). BDNF has been shown to improve the ability of the brain to repair after a stroke ( Liu et al, 2020 ).…”

Section: Association Of Mir-34a With Ischemic Strokementioning

confidence: 99%

Role of microRNA-34a in blood–brain barrier permeability and mitochondrial function in ischemic stroke

Payne,

Tabassum,

et al. 2023

Front. Cell. Neurosci.

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Over the past decade, there has been an uptick in the number of studies conducting research on the role of microRNA (miRNA) molecules in stroke. Among these molecules, miR-34a has emerged as a significant player, as its levels have been observed to exhibit a substantial rise following ischemic events. Elevated levels of miR-34a have been found to have multiple effects, including the modulation of inflammatory molecules involved in the post-stroke recovery process, as well as negative effects on the blood–brain barrier (BBB) permeability. Interestingly, the increase of miR-34a appears to increase BBB permeability post stroke, through the negative effect on mitochondrial function. The strength of mitochondrial function is crucial for limiting para-cellular permeability and maintaining the structural integrity of the BBB. Furthermore, the activation of ischemic repair mechanisms and the reduction of ischemic event damage depend on healthy mitochondrial activity. This review aims to emphasize the involvement of miR-34a in ischemic stroke, specifically its interaction with mitochondrial genes in cerebrovascular endothelial cells, the effect on mitochondrial function, and lastly its regulatory role in BBB permeability. A comprehensive understanding of the role of miR-34a in maintaining BBB integrity and its contribution to the pathogenesis of stroke holds significant value in establishing a foundation for the development of future therapeutics and diagnostic markers.

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Inhibition of miR-34a ameliorates cerebral ischemia/reperfusion injury by targeting brain-derived neurotrophic factor

Cited by 2 publications

References 30 publications

Single Cell sequencing reveals heterogenicity of differential gene-expression and altered interactome in post ischemic mice brain cells

Single Cell sequencing reveals heterogenicity of differential gene-expression and altered interactome in post ischemic mice brain cells

Role of microRNA-34a in blood–brain barrier permeability and mitochondrial function in ischemic stroke

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