miRNA-144 induces microglial autophagy and inflammation following intracerebral hemorrhage

Yu, Anyong; Zhang, Tianxi; Zhong, Wenyi; Duan, Haizhen; Wang, Song; Ye, Peng; Wang, Juan; Zhong, Shanchuan; Yang, Zhao

doi:10.1016/j.imlet.2017.01.002

Cited by 46 publications

(34 citation statements)

References 41 publications

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“…Evidence indicates that miRNAs play an important role in inflammation response, which could mediate gene expression and function 42. Overexpression of miR-146a could alleviate inflammation response in mice with POCD, as evidenced by a decreased level of NF-κB and proinflammatory cytokines (IL-1β and IL-6) 43.…”

Section: Discussionmentioning

confidence: 99%

<p>Dexmedetomidine Attenuates Neuroinflammation In LPS-Stimulated BV2 Microglia Cells Through Upregulation Of miR-340</p>

Yang

Zhu

et al. 2019

DDDT

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BackgroundDexmedetomidine (Dex) was reported to exhibit anti-inflammatory effect in the nervous system. However, the mechanism by which Dex exhibits anti-inflammation effects on LPS-stimulated BV2 microglia cells remains unclear. Thus, this study aimed to investigate the role of Dex in LPS-stimulated BV2 cells.MethodsThe BV2 cells were stimulated by lipopolysaccharides (LPS). BV2 cells were infected with short-hairpin RNAs targeting NF-κB (NF-κB-shRNAs) and NF-κB overexpression lentivirus, respectively. In addition, miR-340 mimics or miR-340 inhibitor was transfected into BV2 cells, respectively. Meanwhile, the dual-luciferase reporter system assay was used to explore the interaction of miR-340 and NF-κB in BV2 cells. CCK-8 was used to detect the viability of BV2 cells. In addition, Western blotting was used to detect the level of NF-κB in LPS-stimulated BV2 cells. The levels of TNF-α, IL-6, IL-1β, IL-2, IL-12, IL-10 and MCP-1 in LPS-stimulated BV2 cells were measured with ELISA.ResultsThe level of miR-340 was significantly upregulated in Dex-treated BV2 cells. Meanwhile, the level of NF-κB was significantly increased in BV2 cells following infection with lenti-NF-κB, which was markedly reversed by Dex. LPS markedly increased the expression of NF-κB and proinflammatory cytokines in BV2 cells, which were reversed in the presence of Dex. Moreover, miR-340 mimics enhanced the anti-inflammatory effects of Dex in LPS-stimulated BV2 cells via inhibiting NF-κB and proinflammatory cytokines. Furthermore, Dex obviously inhibited LPS-induced phagocytosis in BV2 cells.ConclusionTaken together, our results suggested that Dex might exert anti-inflammatory effects in LPS-stimulated BV2 cells via upregulation of miR-340. Therefore, Dex might serve as a potential agent for the treatment of neuroinflammation.

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Section: Discussionmentioning

confidence: 99%

<p>Dexmedetomidine Attenuates Neuroinflammation In LPS-Stimulated BV2 Microglia Cells Through Upregulation Of miR-340</p>

Yang

Zhu

et al. 2019

DDDT

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“…Mediated by HIF-1α (hypoxia-inducible factor 1α), hypoxia-induced autophagy promotes microglia cell death after ICH [90]. The mTOR pathway integrates diverse environmental signals to regulate autophagy, and mTOR upregulation attenuates microglial autophagy and inflammation after ICH [91]. Neutrophil extracellular traps (NETs) are extracellular chromatin structures that trap and degrade microbes [92].…”

Section: Crosstalk Between Autophagy Er Stress and The Uprmentioning

confidence: 99%

Autophagy, endoplasmic reticulum stress and the unfolded protein response in intracerebral hemorrhage

Niu

Dai

Zou

et al. 2017

Translational Neuroscience

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Intracerebral hemorrhage (ICH) is a subtype of stroke that is followed by primary and secondary brain injury. As a result of the injury, cell metabolism is disrupted and a series of stress responses are activated, such as endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), leading to the re-establishment of cell homeostasis or cell death. As an important mechanism of cell homeostasis, autophagy has been widely studied, and the associations between autophagy, ER stress, and the UPR have also been demonstrated. Whether these mechanisms are beneficial or detrimental remains a matter of controversy, but there is no doubt as to their vital functions. An understanding of the mechanisms of injury and recovery after ICH is crucial to develop therapeutic strategies. In this review, we summarize the related studies and highlight the roles of autophagy, ER stress, and the UPR in disease, especially in ICH. We also provide an overview of therapeutic approaches that target autophagy, and we discuss the prospects for modulating autophagy, ER stress, and UPR mechanisms in ICH therapy.

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“…Several studies have found that ICH upregulated the expression level of miRNA-144 but decreased mTOR expression, which lead to increased inflammation and microglial autophagy. Their findings suggested that miRNA-144 was a critical regulator of autophagy by modulating mTOR (113). Later, another study published by Wang et al indicated that miRNA-144 contributed to activated autophagy of microglia through the mTOR signaling pathway, which might be mediated by hemoglobin (114).…”

Section: Secondary Brain Injury-induced Depressionmentioning

confidence: 99%

Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage

Wang

et al. 2018

Front. Psychiatry

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The relationship between depression and intracerebral hemorrhage (ICH) is complicated. One of the most common neuropsychiatric comorbidities of hemorrhagic stroke is Post-ICH depression. Depression, as a neuropsychiatric symptom, also negatively impacts the outcome of ICH by enhancing morbidity, disability, and mortality. However, the ICH outcome can be improved by antidepressants such as the frequently-used selective serotonin reuptake inhibitors. This review therefore presents the mechanisms of post-ICH depression, we grouped the mechanisms according to inflammation, oxidative stress (OS), apoptosis and autophagy, and explained them through their several associated signaling pathways. Inflammation is mainly related to Toll-like receptors (TLRs), the NF-kB mediated signal pathway, the PPAR-γ-dependent pathway, as well as other signaling pathways. OS is associated to nuclear factor erythroid-2 related factor 2 (Nrf2), the PI3K/Akt pathway and the MAPK/P38 pathway. Moreover, autophagy is associated with the mTOR signaling cascade and the NF-kB mediated signal pathway, while apoptosis is correlated with the death receptor-mediated apoptosis pathway, mitochondrial apoptosis pathway, caspase-independent pathways and others. Furthermore, we found that neuroinflammation, oxidative stress, autophagy, and apoptosis experience interactions with one another. Additionally, it may provide several potential therapeutic targets for patients that might suffer from depression after ICH.

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miRNA-144 induces microglial autophagy and inflammation following intracerebral hemorrhage

Cited by 46 publications

References 41 publications

<p>Dexmedetomidine Attenuates Neuroinflammation In LPS-Stimulated BV2 Microglia Cells Through Upregulation Of miR-340</p>

<p>Dexmedetomidine Attenuates Neuroinflammation In LPS-Stimulated BV2 Microglia Cells Through Upregulation Of miR-340</p>

Autophagy, endoplasmic reticulum stress and the unfolded protein response in intracerebral hemorrhage

Mechanisms and Therapeutic Targets of Depression After Intracerebral Hemorrhage

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