Micro<scp>RNA</scp>‐181c negatively regulates the inflammatory response in oxygen‐glucose‐deprived microglia by targeting Toll‐like receptor 4

Zhang, Li; Li, Ya-Jian; Wu, Xunyi; Hong, Zhen; Wei, Wenshi

doi:10.1111/jnc.13021

Cited by 101 publications

(78 citation statements)

References 40 publications

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“…In addition, many other miR181c target genes regulate the cellular viability. It is reported that miR-181c protects neurons against injury under hypoxia by inhibition TLR4 expression, thus inhibiting NF-κB activation and the production of downstream proinflammatory mediators [54]. MiR-181c protects myocardial cells from apoptosis by targeting Bcl-2 protein, one of the anti-apoptotic members of the Bcl-2 family [55].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-181c Ameliorates Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion in Rats

Chen

Min

et al. 2016

Mol Neurobiol

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Chronic cerebral hypoperfusion (CCH) characterized by global cerebral ischemia is an important risk factor contributing to the development of dementia. MicroRNAs (miRNAs) play important roles in the cellular adaptation to long-term ischemia/hypoxia by turning off or on the expression of target genes. MiR-181c is widely expressed in the nervous system, and tripartite motif 2 (TRIM2) is one of its target genes. In this work, we had identified that progressive spatial memory deficiency was induced in the bilateral common carotid artery occlusion (2-VO) rat models. Meanwhile, inhibition of miR-181c expression and upregulation of TRIM2 in the hippocampus of 2-VO rats were found accompanying with reduction in the dendritic branching and dendrite spine density of the hippocampal neurons. Viral vector-mediated miR-181c delivery might improve the cognitive deficiency via TRIM2 on neurofilament light (NF-L) ubiquitination resulting in remodeling of the hippocampal neurons as well as increase in N-methyl-D-aspartate receptor 1 (NR1) subunit cell surface expression. Meanwhile, miR-181c might rescue the cellular activity from ischemia/hypoxia. These results indicated a novel miRNA-mediated mechanism involving miR-181c and TRIM2 in the cognitive impairment induced by CCH and provided a rationale for the development of miRNA-based strategies for prevention of dementia.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-181c Ameliorates Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion in Rats

Chen

Min

et al. 2016

Mol Neurobiol

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“…A recent study identified an important role for the miR-181c-TLR4 pathway in hypoxic microglial activation and neuroinflammation. miR-181c was found to inhibit TLR4 expression by binding to its 3 0 -UTR, thus inhibiting NF-kB activation and the production of downstream proinflammatory mediators [20]. Hence, miR-181c is likely to be of importance in neuroimmunological diseases.…”

Section: Discussionmentioning

confidence: 99%

Decreased microRNA miR-181c expression in peripheral blood mononuclear cells correlates with elevated serum levels of IL-7 and IL-17 in patients with myasthenia gravis

et al. 2015

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miR-181c is a newly identified negative regulator of immune cell activation. In this study, we aimed to investigate the expression and functional role of miR-181c in myasthenia gravis (MG). miR-181c showed significant downregulation in peripheral blood mononuclear cells (PBMCs) from MG patients compared with healthy controls, with lower expression in generalized patients than in ocular ones. MG patients also had increased serum IL-7 and IL-17 levels. Additionally, serum IL-7 level presents a positive correlation with the serum IL-17 level. miR-181c levels were negatively correlated with serum levels of IL-7 and IL-17 in either generalized patients or ocular patients. A luciferase reporter assay revealed that miR-181c could directly bind to the 3'-UTR of interleukin-7. Forced expression of miR-181c led to decreased IL-7 and IL-17 release in cultured PBMCs, while depletion of miR-181c increased the secretion of these two proinflammatory cytokines. The results from our study suggested for the first time that miR-181c was able to negatively regulate the production of proinflammatory cytokines IL-7 and IL-17 in MG patients, and it is a novel potential therapeutic target for MG.

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“…It is determined that miR-181c negatively regulates TLR4 expression through its 3′-UTR. Furthermore, miR-181c suppresses NF-κB activation and its pro-inflammatory products including TNF-α, IL-1β, and iNOS [126]. In ischemic cerebral tissue, miR-155 induces the expression of TNF-α and IL-1β via upregulation of TLR4 and downregulates the expression of inflammatory mediators such as suppressor of cytokine signaling 1 (SOCS1) and the myeloid differentiation primary response gene 88 (MyD88) [127].…”

Section: Micrornas Intervention In Ischemic Stroke Progressionmentioning

confidence: 99%

Emerging Roles of microRNAs in Ischemic Stroke: As Possible Therapeutic Agents

et al. 2017

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Stroke is one of the leading causes of death and physical disability worldwide. The consequences of stroke injuries are profound and persistent, causing in considerable burden to both the individual patient and society. Current treatments for ischemic stroke injuries have proved inadequate, partly owing to an incomplete understanding of the cellular and molecular changes that occur following ischemic stroke. MicroRNAs (miRNA) are endogenously expressed RNA molecules that function to inhibit mRNA translation and have key roles in the pathophysiological processes contributing to ischemic stroke injuries. Potential therapeutic areas to compensate these pathogenic processes include promoting angiogenesis, neurogenesis and neuroprotection. Several miRNAs, and their target genes, are recognized to be involved in these recoveries and repair mechanisms. The capacity of miRNAs to simultaneously regulate several target genes underlies their unique importance in ischemic stroke therapeutics. In this Review, we focus on the role of miRNAs as potential diagnostic and prognostic biomarkers, as well as promising therapeutic agents in cerebral ischemic stroke.

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MicroRNA‐181c negatively regulates the inflammatory response in oxygen‐glucose‐deprived microglia by targeting Toll‐like receptor 4

Cited by 101 publications

References 40 publications

MicroRNA-181c Ameliorates Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion in Rats

MicroRNA-181c Ameliorates Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion in Rats

Decreased microRNA miR-181c expression in peripheral blood mononuclear cells correlates with elevated serum levels of IL-7 and IL-17 in patients with myasthenia gravis

Emerging Roles of microRNAs in Ischemic Stroke: As Possible Therapeutic Agents

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