Inhibition of microRNA-124-3p as a novel therapeutic strategy for the treatment of Gulf War Illness: Evaluation in a rat model

Laferriere, Nicole R; Kurata, Wendy E.; Grayson, Cary T.; Stecklow, Kelsey M.; Pierce, Lisa

doi:10.1016/j.neuro.2018.11.008

Cited by 10 publications

(4 citation statements)

References 98 publications

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“…U6, SnorD96, Snor68, Snor234, and Snor202 were evaluated for stability among groups and SnorD96 was chosen for normalization. SnorD96 has also been used by others[ 39 , 40 ]. Primers were purchased from Qiagen, Maryland.…”

Section: Methodsmentioning

confidence: 99%

Immune and microRNA responses toHelicobacter muridaruminfection and indole-3-carbinol during colitis

Alkarkoushi

Hui

Tavakoli

et al. 2020

WJG

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BACKGROUND Indole-3-carbinol (I3C) and other aryl hydrocarbon receptor agonists are known to modulate the immune system and ameliorate various inflammatory and autoimmune diseases in animal models, including colitis induced by dextran sulfate sodium (DSS). MicroRNAs (miRNAs) are also gaining traction as potential therapeutic agents or diagnostic elements. Enterohepatic Helicobacter (EHH) species are associated with an increased risk of inflammatory bowel disease, but little is known about how these species affect the immune system or response to treatment. AIM To determine whether infection with an EHH species alters the response to I3C and how the immune and miRNA responses of an EHH species compare with responses to DSS and inflammatory bowel disease. METHODS We infected C57BL/6 mice with Helicobacter muridarum ( H. muridarum ), with and without DSS and I3C treatment. Pathological responses were evaluated by histological examination, symptom scores, and cytokine responses. MiRNAs analysis was performed on mesenteric lymph nodes to further evaluate the regional immune response. RESULTS H. muridarum infection alone caused colonic inflammation and upregulated proinflammatory, macrophage-associated cytokines in the colon similar to changes seen in DSS-treated mice. Further upregulation occurred upon treatment with DSS. H. muridarum infection caused broad changes in mesenteric lymph node miRNA expression, but colitis-associated miRNAs were regulated similarly in H. muridarum- infected and uninfected, DSS-treated mice. In spite of causing colitis exacerbation, H. muridarum infection did not prevent disease amelioration by I3C. I3C normalized both macrophage- and T cell-associated cytokines. CONCLUSION Thus, I3C may be useful for inflammatory bowel disease patients regardless of EHH infection. The miRNA changes associated with I3C treatment are likely the result of, rather than the cause of immune response changes.

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Section: Methodsmentioning

confidence: 99%

Immune and microRNA responses toHelicobacter muridaruminfection and indole-3-carbinol during colitis

Alkarkoushi

Hui

Tavakoli

et al. 2020

WJG

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“…Pierce et al established GWI model and found up-regulation of miR-124-3p and miR-29b-3p expression in rat hippocampus. Subsequent researches have demonstrated that intracerebroventricular miR-124 antisense oligonucleotide injection leads to down-regulated miR-124 expression and up-regulated a variety of proteins closely related to cognitive dysfunction such as neurogenesis, memory, anxiety disorder, depression, which have been identified as miR-124 targets to improve GWI cognitive impairment (Pierce et al 2016 ; Laferriere et al 2019 ).…”

Section: Mir-124 In Cognitionmentioning

confidence: 99%

MicroRNA‑124: an emerging therapeutic target in central nervous system disorders

Zhang

Lian

et al. 2023

Exp Brain Res

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The central nervous system (CNS) consists of neuron and non-neuron cells including neural stem/precursor cells (NSPCs), neuroblasts, glia cells (mainly astrocyte, oligodendroglia and microglia), which thereby form a precise and complicated network and exert diverse functions through interactions of numerous bioactive ingredients. MicroRNAs (miRNAs), with small size approximately ~ 21nt and as well-documented post-transcriptional key regulators of gene expression, are a cluster of evolutionarily conserved endogenous non-coding RNAs. More than 2000 different miRNAs has been discovered till now. MicroRNA-124(miR-124), the most brain-rich microRNA, has been validated to possess important functions in the central nervous system, including neural stem cell proliferation and differentiation, cell fate determination, neuron migration, synapse plasticity and cognition, cell apoptosis etc. According to recent studies, herein, we provide a review of this conversant miR-124 to further understand the potential functions and therapeutic and clinical value in brain diseases.

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“…The biological function of miR-124-3p is similar to other members of the miR-124 family. According to reports, miR-124-3p is involved in the occurrence and development of various diseases [15][16][17][18][19][20][21][22]. For example, miR-124-3p was reported to regulate the neural development and was an enriched miRNA in brain [15,16].…”

Section: Introductionmentioning

confidence: 99%

“…The expression of miR-124-3p is significantly reduced in Alzheimer's disease (AD) and other neurodegenerative diseases [20]. In addition, miR-124-3p was reported to be involved in other diseases [21,22]. However, it is not clear whether miR-124-3p can regulate the pathogenesis of HIE.…”

Section: Introductionmentioning

confidence: 99%

Role of microRNA-124-3p/Bax axis in neonatal hypoxic-ischaemic encephalopathy

Chen

Wang

Luo

et al. 2020

Biotechnology & Biotechnological Equipment

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Neonatal hypoxic-ischaemic encephalopathy (HIE) is a neurological disease that can cause neonatal death. plays an important role in the development of various diseases. In this research, our aim was to investigate the potential function of miR-124-3p in regulating HIE and to find the underlying mechanism. Here, we discovered that miR-124-3p expression was reduced and cell apoptosis was increased in HIE rat model group. Interestingly, we identified that B cell lymphoma-2-associated X protein (Bax) was a direct target gene of miR-124-3p and Bax expression was negatively modulated by miR-124-3p in HIE. Functional experiments showed that miR-124-3p expression was reduced and Bax expression was increased in oxygen and glucose deprivation (OGD)-treated neurons. In addition, the cell viability of neurons was decreased and apoptosis was increased after OGD treatment. And miR-124-3p over-expression promoted cell viability and restrained apoptosis of the OGD-treated neurons. All these effects were reversed by Bax over-expression. Our results indicated that over-expression of miR-124-3p attenuated OGD-induced neuronal injury through targeting Bax, suggesting a potential role of miR-124-3p/Bax in the pathophysiology of HIE.

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Inhibition of microRNA-124-3p as a novel therapeutic strategy for the treatment of Gulf War Illness: Evaluation in a rat model

Cited by 10 publications

References 98 publications

Immune and microRNA responses toHelicobacter muridaruminfection and indole-3-carbinol during colitis

Immune and microRNA responses toHelicobacter muridaruminfection and indole-3-carbinol during colitis

MicroRNA‑124: an emerging therapeutic target in central nervous system disorders

Role of microRNA-124-3p/Bax axis in neonatal hypoxic-ischaemic encephalopathy

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