Emerging Role of MicroRNA-30c in Neurological Disorders

Kumar, Manish; Li, Guohong

doi:10.3390/ijms24010037

Cited by 8 publications

(7 citation statements)

References 114 publications

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“…Reduced gene expression was mainly concentrated in pathways associated with nicotine addiction and neuroactive ligand-receptor interaction.. More than 100 different microRNAs (miRNAs) have been detected and identi ed in the bloodstream of people who are in good health. (Kumar and Li 2022). In biology, let-7 is the most studied miRNA, in addition to the let-7, The regulation of differentiation and pluripotency in many animals is largely dependent on the Mir family member.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of serum miR 155 and miR 30c as a Potential Biomarker for Alzheimer’s Disease

Kafshdooz,

Farajnia,

Sharifi

et al. 2024

Preprint

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Alzheimer's disease (AD), the most common type of dementia, is a serious neurodegenerative disorder for which there is currently no cure. However, available medications can help alleviate the symptoms of the disease. Therefore, it is essential to promptly and accurately diagnose the condition and understand the molecular mechanisms involved in its progression. Disruption of microRNAs (miRNAs) is implicated in the development of neurodegenerative conditions, such as Alzheimer's disease (AD). The research was carried out in order to determine the significance of Mir 30c, and Mir 155 in serving as a diagnostic biomarker The microarray data set GSE138260 was obtained from the Gene Expression Omnibus (GEO) database hosted by the National Center for Biotechnology Information (NCBI) In order to determine gene ontologies, pathways, and networks, one must conduct a comprehensive analysis Blood samples were collected from 30 individuals with AD and 30 individuals without the condition. RNA was extracted from the serum samples, converted to cDNA, and then the real-time PCR method was used to measure the expression level of Mir 30c and Mir 155 . The study's findings indicated that the copy number levels of copy number levels of Mir 30c and Mir 155 were increased. Bioinformatics analysis revealed that these microRNA target pathways are associated with Alzheimer's disease. The cut-off value for this Mir´s demonstrates the trade-off between sensitivity and specificity in diagnostic testing.

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Section: Discussionmentioning

confidence: 99%

Upregulation of serum miR 155 and miR 30c as a Potential Biomarker for Alzheimer’s Disease

Kafshdooz,

Farajnia,

Sharifi

et al. 2024

Preprint

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“…This comparison confirmed that the modulated miRNAs were involved in inflammatory and immune pathways ( Supplementary Table S1 ), including relevant upregulated genes such as miR-155-5p and miR-186-5p, which are downregulated in elderly people and those with a neurodegenerative disease ( 26 , 38 ). The upregulation of miR-30c, previously implicated in MS ( 39 ) and characterized in response to pharmacological treatments ( 19 , 40 ), together with the downregulation of miR-199a in the MS relapsing phase is correlated with more frequent Th17 cell differentiation and the severity of the disease ( 41 ). These data suggest a more inflammatory profiling of the patients selected for CLA compared to the pre-OCRE ones, supporting the possible use of miRNAs for a personalized DMT choice.…”

Section: Discussionmentioning

confidence: 99%

Cladribine and ocrelizumab induce differential miRNA profiles in peripheral blood mononucleated cells from relapsing–remitting multiple sclerosis patients

Arisi,

Malimpensa,

Manzini

et al. 2023

Front. Immunol.

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Background and objectivesMultiple sclerosis (MS) is a chronic, progressive neurological disease characterized by early-stage neuroinflammation, neurodegeneration, and demyelination that involves a spectrum of heterogeneous clinical manifestations in terms of disease course and response to therapy. Even though several disease-modifying therapies (DMTs) are available to prevent MS-related brain damage—acting on the peripheral immune system with an indirect effect on MS lesions—individualizing therapy according to disease characteristics and prognostic factors is still an unmet need. Given that deregulated miRNAs have been proposed as diagnostic tools in neurodegenerative/neuroinflammatory diseases such as MS, we aimed to explore miRNA profiles as potential classifiers of the relapsing–remitting MS (RRMS) patients’ prospects to gain a more effective DMT choice and achieve a preferential drug response.MethodsA total of 25 adult patients with RRMS were enrolled in a cohort study, according to the latest McDonald criteria before (pre-cladribine, pre-CLA; pre-ocrelizumab, pre-OCRE, time T0) and after high-efficacy DMTs, time T1, 6 months post-CLA (n = 10, 7 F and 3 M, age 39.0 ± 7.5) or post-OCRE (n = 15, 10 F and 5 M, age 40.5 ± 10.4) treatment. A total of 15 age- and sex-matched healthy control subjects (9 F and 6 M, age 36.3 ± 3.0) were also selected. By using Agilent microarrays, we analyzed miRNA profiles from peripheral blood mononuclear cells (PBMC). miRNA–target networks were obtained by miRTargetLink, and Pearson’s correlation served to estimate the association between miRNAs and outcome clinical features.ResultsFirst, the miRNA profiles of pre-CLA or pre-OCRE RRMS patients compared to healthy controls identified modulated miRNA patterns (40 and seven miRNAs, respectively). A direct comparison of the two pre-treatment groups at T0 and T1 revealed more pro-inflammatory patterns in the pre-CLA miRNA profiles. Moreover, both DMTs emerged as being capable of reverting some dysregulated miRNAs toward a protective phenotype. Both drug-dependent miRNA profiles and specific miRNAs, such as miR-199a-3p, miR-29b-3p, and miR-151a-3p, emerged as potentially involved in these drug-induced mechanisms. This enabled the selection of miRNAs correlated to clinical features and the related miRNA–mRNA network.DiscussionThese data support the hypothesis of specific deregulated miRNAs as putative biomarkers in RRMS patients’ stratification and DMT drug response.

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“…1,2 These diseases encompass various ailments: Parkinson's disease (PD), migraine headache, Alzheimer's disease (AD), multiple sclerosis, seizure disorder, as well as cerebrovascular accidents. 3 NDs can cause slow and progressive deformations, leading to the loss of neurons and synapses. "Protein misfolding" diseases or proteinopathies are now the terms best describing the essential etiologies of NDs and defining these conditions.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Neurological disorders (NDs) are clinically characterized as pathologies that influence the cerebrum and the nerves that comprise the central and peripheral neural networks 1,2 . These diseases encompass various ailments: Parkinson's disease (PD), migraine headache, Alzheimer's disease (AD), multiple sclerosis, seizure disorder, as well as cerebrovascular accidents 3 …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuroprotective effects of gemfibrozil in neurological disorders: Focus on inflammation and molecular mechanisms

Ivraghi,

Zamanian,

Gupta

et al. 2023

CNS Neurosci Ther

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BackgroundGemfibrozil (Gem) is a drug that has been shown to activate PPAR‐α, a nuclear receptor that plays a key role in regulating lipid metabolism. Gem is used to lower the levels of triglycerides and reduce the risk of coronary heart disease in patients. Experimental studies in vitro and in vivo have shown that Gem can prevent or slow the progression of neurological disorders (NDs), including cerebral ischemia (CI), Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Neuroinflammation is known to play a significant role in these disorders.MethodThe literature review for this study was conducted by searching Scopus, Science Direct, PubMed, and Google Scholar databases.ResultThe results of this study show that Gem has neuroprotective effects through several cellular and molecular mechanisms such as: (1) Gem has the ability to upregulate pro‐survival factors (PGC‐1α and TFAM), promoting the survival and function of mitochondria in the brain, (2) Gem strongly inhibits the activation of NF‐κB, AP‐1, and C/EBPβ in cytokine‐stimulated astroglial cells, which are known to increase the expression of iNOS and the production of NO in response to proinflammatory cytokines, (3) Gem protects dopamine neurons in the MPTP mouse model of PD by increasing the expression of PPARα, which in turn stimulates the production of GDNF in astrocytes, (4) Gem reduces amyloid plaque pathology, reduces the activity of glial cells, and improves memory, (5) Gem increases myelin genes expression (MBP and CNPase) via PPAR‐β, and (6) Gem increases hippocampal BDNF to counteract depression.ConclusionAccording to the study, Gem was investigated for its potential therapeutic effect in NDs. Further research is needed to fully understand the therapeutic potential of Gem in NDs.

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Emerging Role of MicroRNA-30c in Neurological Disorders

Cited by 8 publications

References 114 publications

Upregulation of serum miR 155 and miR 30c as a Potential Biomarker for Alzheimer’s Disease

Upregulation of serum miR 155 and miR 30c as a Potential Biomarker for Alzheimer’s Disease

Cladribine and ocrelizumab induce differential miRNA profiles in peripheral blood mononucleated cells from relapsing–remitting multiple sclerosis patients

Neuroprotective effects of gemfibrozil in neurological disorders: Focus on inflammation and molecular mechanisms

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