Effects of miR-26a-5p on neuropathic pain development by targeting MAPK6 in in CCI rat models

Zhang, Yang; Su, Zhen; Liu, Hailin; Lin, Li; Wang, Meng; Ge, Dong-Jian; Zhang, Zhijie

doi:10.1016/j.biopha.2018.08.005

Cited by 46 publications

(28 citation statements)

References 32 publications

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“…In addition, miR-26a-5p is considered to be associated with inflammation and apoptosis in numerous diseases. For example, the overexpression of miR-26a-5p could markedly suppress neuropathic pain and neuroinflammation in rats with chronic sciatic nerve injury (30). Wen et al (31) have suggested that miR-26a-5p significantly decreased myocardial cell apoptosis and expression of inflammatory factors in acute myocardial infarction by targeting ADAM17.…”

Section: Discussionmentioning

confidence: 99%

miR‑26a‑5p alleviates lipopolysaccharide‑induced acute lung injury by targeting the connective tissue growth factor

Yang

Fei

2020

Mol Med Rep

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The aim of the present study was to investigate the regulatory functions of microRNA (miR)-26a-5p on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and its molecular mechanisms. The role of miR-26a-5p on an ALI mouse model was evaluated by examining the histological changes, wet/dry (W/D) ratio, myeloperoxidase (MPO) activity, malondialdehyde (MDA) expression levels in lung tissues and the survival of ALI mice. Moreover, the protein concentration and the number of neutrophils and lymphocytes in bronchoalveolar lavage fluid (BALF) was analyzed. To explore the effect of miR-26a-5p on inflammatory responses and apoptosis, the expression levels of tumour necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 and apoptosis were measured by ELISA, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling staining and flow cytometry in BALF, A549 cells and lung tissues. B-cell lymphoma-2 (Bcl-2), Bax and cleaved caspase-3 in lung tissues were measured by western blotting and reverse transcription-quantitative PCR. Connective tissue growth factor (CTGF) was predicted as a direct target of miR-26a-5p using dual luciferase reporter assay. The present study sought to determine whether CTGF overexpression reversed the effect of miR-26a-5p on apoptosis and inflammatory responses in LPS-induced A549 cells. The data revealed that miR-26a-5p overexpression ameliorated LPS-induced ALI, which was implicated by fewer histopathological changes, W/D ratio, apoptosis in lung tissues and the survival of ALI mice. Moreover, miR-26a-5p overexpression alleviated LPS-induced inflammatory responses in ALI mice via the reduction of total protein, neutrophil and lymphocyte counts and the expression levels of TNF-α, IL-1β, IL-6, MDA and MPO activity in BALF. Similarly, miR-26a-5p overexpression decreased apoptosis and the expression of TNF-α, IL-1β and IL-6 in LPS-induced A549 cells. CTGF was a direct target of miR-26a-5p. CTGF overexpression reversed the effect of miR-26a-5p on cell apoptosis and inflammatory responses in LPS-induced A549 cells. The present study demonstrated that miR-26a-5p could attenuate lung inflammation and apoptosis in LPS-induced ALI by targeting CTGF.

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Section: Discussionmentioning

confidence: 99%

miR‑26a‑5p alleviates lipopolysaccharide‑induced acute lung injury by targeting the connective tissue growth factor

Yang

Fei

2020

Mol Med Rep

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“…In the absence of a background of stress, miRNAs have been hypothesized to influence anxiety-like behavior potentially through metabolic or inflammatory mechanisms as several miRNAs, for example mir-34c and mir-26a family miRNAs, are implicated in both changes in inflammation and the modulation of anxiety-like behavior [23,24,44]. Inflammation is traditionally associated with enhanced anxiety [45], and consistently, mir26a has been shown to be anti-inflammatory and anxiolytic [24,46]. Future studies could explore the role of other putative targets of mir-598-3p involved in inflammation to better understand its potential role in anxiety in either naïve or stress-resilient mice.…”

Section: Discussionmentioning

confidence: 99%

microRNA mir-598-3p mediates susceptibility to stress-enhancement of remote fear memory

Jones

Sillivan

Jamieson

et al. 2019

Preprint

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Number of words in abstract: 214Number of words in main text: 5,913Running title: BLA mir-598-3p supports stress-enhanced memory ABSTRACT microRNAs (miRNAs) have emerged as potent regulators of learning, recent memory and extinction. However, our understanding of miRNAs directly involved in regulating complex psychiatric conditions perpetuated by aberrant memory, such as in posttraumatic stress disorder (PTSD), remains limited. To begin to address the role of miRNAs in persistent memory, we performed small-RNA sequencing on basolateral amygdala (BLA) tissue to identify miRNAs altered by auditory fear conditioning (FC) one month after training. mir-598-3p, a highly conserved miRNA previously unstudied in the brain, was downregulated in the BLA. Further decreasing BLA mir-598-3p levels did not alter the expression or extinction of the remote fear memory. Given that stress is a critical component in PTSD, we next assessed the impact of stress-enhanced fear learning (SEFL) on mir-598-3p levels, finding the miRNA is elevated in the BLA of male, but not female, mice susceptible to the effects of stress in SEFL. Accordingly, intra-BLA inhibition of mir-598-3p interfered with expression and extinction of the remote fear memory in male, but not female, mice. This effect could not be attributed to an anxiolytic effect of miRNA inhibition. Finally, bioinformatic analysis following quantitative proteomics on BLA tissue collected 30 days post-SEFL training identified putative mir-598-3p targets and related pathways mediating the differential susceptibility, with evidence for regulation of the actin cytoskeleton.

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“…Therefore, the down-regulation of miR-362-3p targeting Pax2 may rather be a compensatory change to restore GABAergic signaling in the SDH [112]. These processes are further enhanced by the down-regulation of three miRNAs (miR-20b-5p, miR-23 and miR-26a-5p) leading to the increased expression of the kinases Akt3, Nox4 and Mapk6 whose relevance for neuropathic pain is well accepted [89,92,93]. Together, miRNAs are emerging as major controllers of neuro-immune processes in the SDH by switching neurons as well as non-neuronal cells into proalgesic modes of action and promoting the development and maintenance of signatures aggravating neuropathic pain at spinal cord level.…”

Section: Mirnas Deregulated In the Peripheral Nervementioning

confidence: 99%

Non-coding RNAs in neuropathic pain

2020

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Neuro-immune alterations in the peripheral and central nervous system play a role in the pathophysiology of chronic pain in general, and members of the non-coding RNA (ncRNA) family, specifically the short, 22 nucleotide microRNAs (miRNAs) and the long non-coding RNAs (lncRNAs) act as master switches orchestrating both immune as well as neuronal processes. Several chronic disorders reveal unique ncRNA expression signatures, which recently generated big hopes for new perspectives for the development of diagnostic applications. lncRNAs may offer perspectives as candidates indicative of neuropathic pain in liquid biopsies. Numerous studies have provided novel mechanistic insight into the role of miRNAs in the molecular sequelae involved in the pathogenesis of neuropathic pain along the entire pain pathway. Specific processes within neurons, immune cells, and glia as the cellular components of the neuropathic pain triad and the communication paths between them are controlled by specific miRNAs. Therefore, nucleotide sequences mimicking or antagonizing miRNA actions can provide novel therapeutic strategies for pain treatment, provided their human homologues serve the same or similar functions. Increasing evidence also sheds light on the function of lncRNAs, which converge so far mainly on purinergic signalling pathways both in neurons and glia, and possibly even other ncRNA species that have not been explored so far.

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Effects of miR-26a-5p on neuropathic pain development by targeting MAPK6 in in CCI rat models

Cited by 46 publications

References 32 publications

miR‑26a‑5p alleviates lipopolysaccharide‑induced acute lung injury by targeting the connective tissue growth factor

miR‑26a‑5p alleviates lipopolysaccharide‑induced acute lung injury by targeting the connective tissue growth factor

microRNA mir-598-3p mediates susceptibility to stress-enhancement of remote fear memory

Non-coding RNAs in neuropathic pain

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