MicroRNA in ischemic stroke

Айтбаев, К. А.; Муркамилов, И Т; Fоmin, Victоr; Муркамилова, Ж. А.; Yusupov, F. A.

doi:10.17116/jnevro20181183248-56

Cited by 10 publications

(6 citation statements)

References 88 publications

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“…MiRNAs dysregulation causes various diseases [ 38 , 39 ]. An increasing number of studies have reported that miRNAs are involved in human cancer [ 40 ], ischemic stroke [ 41 ] and neurodegenerative disorders [ 42 ]. However, the significance of miRNA regulation in the treatment of morphine tolerance remains unclear.…”

Section: Discussionmentioning

confidence: 99%

AMPK-autophagy-mediated inhibition of microRNA-30a-5p alleviates morphine tolerance via SOCS3-dependent neuroinflammation suppression

Wan

Jia

et al. 2022

J Neuroinflammation

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Background The development of morphine tolerance is a clinical challenge for managing severe pain. Studies have shown that neuroinflammation is a critical aspect for the development of analgesic tolerance. We found that AMPK-autophagy activation could suppress neuroinflammation and improve morphine tolerance via the upregulation of suppressor of cytokine signaling 3 (SOCS3) by inhibiting the processing and maturation of microRNA-30a-5p. Methods CD-1 mice were utilized for the tail-flick test to evaluate morphine tolerance. The microglial cell line BV-2 was utilized to investigate the mechanism of AMPK-autophagy-mediated posttranscriptional regulation of SOCS3. Proinflammatory cytokines were measured by western blotting and real-time PCR. The levels of SOCS3 and miRNA-processing enzymes were evaluated by western blotting, real-time PCR and immunofluorescence staining. Results Based on experimental verification, miRNA-30a-5p could negatively regulate SOCS3. The AMPK activators AICAR, resveratrol and metformin downregulated miRNA-30a-5p. We found that AMPK activators specifically inhibited the processing and maturation of miRNA-30a-5p in microglia by degrading DICER and AGO2 via autophagy. Furthermore, a miRNA-30a-5p inhibitor significantly improved morphine tolerance via upregulation of SCOS3 in mice. It markedly increased the level of SOCS3 in the spinal cord of mice and subsequently inhibited morphine-induced phosphorylation of NF-κB p65. In addition, a miRNA-30a-5p inhibitor decreased the levels of IL-1β and TNF-α caused by morphine in microglia. Conclusion AMPK-autophagy activation suppresses neuroinflammation and improves morphine tolerance via the upregulation of SOCS3 by inhibiting miRNA-30a-5p.

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Section: Discussionmentioning

confidence: 99%

AMPK-autophagy-mediated inhibition of microRNA-30a-5p alleviates morphine tolerance via SOCS3-dependent neuroinflammation suppression

Wan

Jia

et al. 2022

J Neuroinflammation

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“…It suggested that miR-140-5p could inhibit neuronal injury, improve neuron function, and suppress the development of ischemic injury. The effects of miRNAs on the regulation of experimental stroke and in the development of carotid artery stroke, as well as functioning as promising biomarkers of stroke have been reported [35]. Besides, miRNAs have emerged as potential diagnostic and prognostic biomarkers in ischemic stroke has also been discussed [36].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of microRNA-140-5p on Ischemic Stroke in Mice via its Regulation on the TLR4/NF-κB Axis

Song

Wang

Shi

et al. 2020

Preprint

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Background and aim: Ischemic stroke is one of the main causes of death worldwide and permanent global disability. On the basis of existing literature data, we carried out studies in an effort to explore how miR-140-5p affects ischemic stroke and whether the mechanism relates to toll-like receptor-4 (TLR4) and nuclear factor-kappa B (NF-κB).Methods: Middle cerebral artery occlusion (MCAO) was employed to establish a mouse model of ischemic stroke in vivo, while primary neurons were exposed to oxygen-glucose deprivation (OGD) to set up an ischemic stroke model in vitro. RT-qPCR was performed to detect the miR-140-5p expression and Western blot was employed to detect the expression TLR4, NF-κB, and apoptosis-related factors. Then, based gain-function of experiments using miR-140-5p mimic and TLR4 overexpression plasmid, neurological function score, TTC staining, TUNEL staining, as well as flow cytometry were carried out to evaluate the effects of miR-140-5p and TLR4 on MCAO mice and OGD neurons. Meanwhile, dual-luciferase reporter assay was used to validate the relationship between miR-140-5p and TLR4.Results: miR-140-5p expressed at a low level and TLR4 at a high level in ischemic stroke. It was verified that miR-140-5p targeted TLR4 and downregulated its expression. miR-140-5p overexpression was observed to inhibit the apoptosis of neurons under OGD exposure and restrain the progression of ischemic stroke, while TLR4 overexpression promoted the apoptosis and disease progression. Besides, miR-140-5p overexpression led to a decrease in NF-κB protein level, which was increased by TLR4 overexpression. Conclusion: In conclusion, from our data we conclude that miR-140-5p overexpression may be instrumental for the therapeutic targeting of ischemic stroke by alleviating neuron injury with the involvement of TLR4/NF-κB axis.

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“…и для богатых холестерином липопротеинов. ЛНП, липопротеины очень низкой плотности и липопротеины промежуточной плотности проникают в субэндотелиальное пространство посредством трансцитоза, где они накапливаются и подвергаются окислению [1,17]. В свою очередь, гипергликемия способствует увеличению циркулирующих нейтрофилов и моноцитов посредством влияния на миелопоэз [1].…”

Section: патофизиологические механизмы развития ссз у пациентов с пре...unclassified

Prediabetes: a risk factor for cardiovascular diseases and a window of opportunity for their prevention

Demidova

Plakhotnyaya²

2023

jour

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It’s well known, that diabetes mellitus predisposes to more rapid development and progression of cardiovascular disease (CVD) and cardiomyopathy. However, the pathological changes underlying them begin to form much earlier — at the stage of prediabetes. Individuals with prediabetes have a higher risk of atherosclerosis and chronic heart failure, as well as increased rates of mortality from CVD and all-cause death. This review is devoted to the analysis of pathophysiological mechanisms that lead to developing CVD in patients with early prediabetes. In addition, the article highlights the issues of preventing the development of cardiovascular pathology in this group of patients with an emphasis on the active impact on the main factors of cardiovascular risk.

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MicroRNA in ischemic stroke

Cited by 10 publications

References 88 publications

AMPK-autophagy-mediated inhibition of microRNA-30a-5p alleviates morphine tolerance via SOCS3-dependent neuroinflammation suppression

AMPK-autophagy-mediated inhibition of microRNA-30a-5p alleviates morphine tolerance via SOCS3-dependent neuroinflammation suppression

Neuroprotective Effects of microRNA-140-5p on Ischemic Stroke in Mice via its Regulation on the TLR4/NF-κB Axis

Prediabetes: a risk factor for cardiovascular diseases and a window of opportunity for their prevention

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