miR‑155 mediates inflammatory injury of hippocampal neuronal cells via the activation of microglia

Sun, Xiaohua; Song, Ming‐Fen; Song, Hai‐Dong; Wang, Yu‑Wen; Luo, Ming‐Jin; Liang, Yin

doi:10.3892/mmr.2019.9917

Cited by 17 publications

(12 citation statements)

References 44 publications

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“…Although the expression of these miRNAs is known from macrophages, their investigation in microglia is still in its beginning. In the case of miR-155, its proinflammatory role in the microglia has been confirmed [ 118 , 119 , 120 , 121 ]. It was also concluded to favor M1 polarization in microglia, and its suppression was associated with polarization to M2 [ 121 ].…”

Section: Melatonin and Micrornas: Relevance To Microgliamentioning

confidence: 99%

Melatonin and Microglia

Hardeland

2021

IJMS

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Melatonin interacts in multiple ways with microglia, both directly and, via routes of crosstalk with astrocytes and neurons, indirectly. These effects of melatonin are of relevance in terms of antioxidative protection, not only concerning free-radical detoxification, but also in prevention of processes that cause, promote, or propagate oxidative stress and neurodegeneration, such as overexcitation, toxicological insults, viral and bacterial infections, and sterile inflammation of different grades. The immunological interplay in the CNS, with microglia playing a central role, is of high complexity and includes signaling toward endothelial cells and other leukocytes by cytokines, chemokines, nitric oxide, and eikosanoids. Melatonin interferes with these processes in multiple signaling routes and steps. In addition to canonical signal transduction by MT1 and MT2 melatonin receptors, secondary and tertiary signaling is of relevance and has to be considered, e.g., via the upregulation of sirtuins and the modulation of pro- and anti-inflammatory microRNAs. Many details concerning the modulation of macrophage functionality by melatonin are obviously also applicable to microglial cells. Of particular interest is the polarization toward M2 subtypes instead of M1, i.e., in favor of being anti-inflammatory at the expense of proinflammatory activities, which is well-documented in macrophages but also applies to microglia.

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Section: Melatonin and Micrornas: Relevance To Microgliamentioning

confidence: 99%

Melatonin and Microglia

Hardeland

2021

IJMS

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“…The study conducted on mice cell lines revealed a possible role of miR-155 in the context of treatment-resistant depression. miR-155 down-regulated SOCS1, leading to the activation of microglia that contributes to inflammatory injury of hippocampal neurons [ 114 ]. In contrast, the correlation analysis of miR-155 expression in RR-MS patients (in the remission phase) with the Beck Depression Index (BDI) scale and with Montreal Cognitive Assessment (MoCA) values did not reveal to be statistically significant [ 74 ].…”

Section: Mir-155 and Neuropsychiatric Symptomsmentioning

confidence: 99%

miR-155 as an Important Regulator of Multiple Sclerosis Pathogenesis. A Review

Maciak

Dziedzic

Miller

et al. 2021

IJMS

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Multiple sclerosis (MS) is a chronic, immune-mediated disease and the leading cause of disability among young adults. MicroRNAs (miRNAs) are involved in the post-transcriptional regulation of gene expression. Of them, miR-155 is a crucial regulator of inflammation and plays a role in modulating the autoimmune response in MS. miR-155 is involved in blood–brain barrier (BBB) disruption via down-regulation of key junctional proteins under inflammatory conditions. It drives demyelination processes by contributing to, e.g., microglial activation, polarization of astrocytes, and down-regulation of CD47 protein and affecting crucial transcription factors. miR-155 has a huge impact on the development of neuropathic pain and indirectly influences a regulatory T (Treg) cell differentiation involved in the alleviation of pain hypersensitivity. This review also focused on neuropsychiatric symptoms appearing as a result of disease-associated stressors, brain atrophy, and pro-inflammatory factors. Recent studies revealed the role of miR-155 in regulating anxiety, stress, inflammation in the hippocampus, and treatment-resistant depression. Inhibition of miR-155 expression was demonstrated to be effective in preventing processes involved in the pathophysiology of MS. This review aimed to support the better understanding the great role of miR-155 dysregulation in various aspects of MS pathophysiology and highlight future perspectives for this molecule.

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“…Elevations in miR-155 are evident in COVID-19 high-risk, pre-existent conditions, including obesity [ 84 ], type II diabetes [ 85 ], hypertension and CVDs [ 86 ], and most human cancers [ 87 ]. Raised miR-155 levels promotes inflammatory cytokine production in macrophages and microglia, in association with a decrease in sirtuin-1 [ 88 ], linking increased miR-155 to a heightened and prolonged ‘cytokine storm’, including from a primed elevation of miR-155 in high-risk conditions. Preclinical data show the raised miR-155 levels in immune cells to accelerate ageing and decrease longevity via an increase in aerobic glycolysis and associated induction of pro-inflammatory processes [ 89 ].…”

Section: Ahr and Wider Covid-19 Pathophysiologymentioning

confidence: 99%

Aryl Hydrocarbon Receptor Role in Co-Ordinating SARS-CoV-2 Entry and Symptomatology: Linking Cytotoxicity Changes in COVID-19 and Cancers; Modulation by Racial Discrimination Stress

Anderson¹,

Carbone

Mazzoccoli

2020

Biology

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There is an under-recognized role of the aryl hydrocarbon receptor (AhR) in co-ordinating the entry and pathophysiology of the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) that underpins the COVID-19 pandemic. The rise in pro-inflammatory cytokines during the ‘cytokine storm’ induce indoleamine 2,3-dioxygenase (IDO), leading to an increase in kynurenine that activates the AhR, thereby heightening the initial pro-inflammatory cytokine phase and suppressing the endogenous anti-viral response. Such AhR-driven changes underpin the heightened severity and fatality associated with pre-existent high-risk medical conditions, such as type II diabetes, as well as to how racial discrimination stress contributes to the raised severity/fatality in people from the Black Asian and Minority Ethnic (BAME) communities. The AhR is pivotal in modulating mitochondrial metabolism and co-ordinating specialized, pro-resolving mediators (SPMs), the melatonergic pathways, acetyl-coenzyme A, and the cyclooxygenase (COX) 2-prostaglandin (PG) E2 pathway that underpin ‘exhaustion’ in the endogenous anti-viral cells, paralleling similar metabolic suppression in cytolytic immune cells that is evident across all cancers. The pro-inflammatory cytokine induced gut permeability/dysbiosis and suppression of pineal melatonin are aspects of the wider pathophysiological underpinnings regulated by the AhR. This has a number of prophylactic and treatment implications for SARS-CoV-2 infection and cancers and future research directions that better investigate the biological underpinnings of social processes and how these may drive health disparities.

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miR‑155 mediates inflammatory injury of hippocampal neuronal cells via the activation of microglia

Cited by 17 publications

References 44 publications

Melatonin and Microglia

Melatonin and Microglia

miR-155 as an Important Regulator of Multiple Sclerosis Pathogenesis. A Review

Aryl Hydrocarbon Receptor Role in Co-Ordinating SARS-CoV-2 Entry and Symptomatology: Linking Cytotoxicity Changes in COVID-19 and Cancers; Modulation by Racial Discrimination Stress

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