miRNA expression is highly sensitive to a drug therapy in Parkinson's disease

Alieva, Anelya Kh.; Filatova, Elena V.; Karabanov, Alexander; Иллариошкин, С. Н.; Limborska, Svetlana A.; Шадрина, М. И.; Slominsky, Petr

doi:10.1016/j.parkreldis.2014.10.018

Cited by 61 publications

(61 citation statements)

References 13 publications

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“…31 Consistent with these results, a previous study also demonstrated that the expression of MALAT1 was increased in the midbrain tissues of mice suffering from MPTP-induced PD. 33 Furthermore, computational analyses have predicted that two miRNAs, miR-129-5p, and miR-142-3p, might be involved in the regulation of MALAT1 and HMGB1, 18 because MALAT1 enhanced the growth of OS cells and increased the expression of HMGB1 by suppressing the expression of miR-129-5p and miR-142-3p. 33 Furthermore, computational analyses have predicted that two miRNAs, miR-129-5p, and miR-142-3p, might be involved in the regulation of MALAT1 and HMGB1, 18 because MALAT1 enhanced the growth of OS cells and increased the expression of HMGB1 by suppressing the expression of miR-129-5p and miR-142-3p.…”

Section: Discussionmentioning

confidence: 99%

Administration of resveratrol improved Parkinson’s disease‐like phenotype by suppressing apoptosis of neurons via modulating the MALAT1/miR‐129/SNCA signaling pathway

Xia

Sui

Zhang

2018

J of Cellular Biochemistry

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Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in the pathogenesis of Parkinson’s disease (PD). In addition, resveratrol was shown to regulate the expression of MALAT1. Therefore, the objective of this study was to clarify the role of resveratrol in PD. During the study, luciferase assays were conducted to determine the effect of resveratrol on the transcription efficiency of MALAT1 promoter as well as the regulatory relationships among MALAT1, miR‐129, and SNCA. In addition, real‐time PCR, Western blot analysis, MTT and flow cytometry analyses were conducted to investigate the mechanism of resveratrol in PD. Furthermore, a PD mouse model was established to study the role of resveratrol in vivo. It was found that resveratrol increased the number of TH+ cells and the expression of miR‐129, while decreasing the expression of MALAT1 and SNCA. In addition, MALAT1 inhibited the expression of miR‐129, a negative regulator of SNCA, thus increasing the expression of SNCA. A further mechanistic study revealed that resveratrol inhibited MALAT1 expression by blocking the transcription of the MALAT1 promoter. Finally, MPTP treatment could decrease cell proliferation and increase cell apoptosis, while resveratrol could partly offset the effect of MPTP. In summary, the therapeutic effect of resveratrol in the treatment of PD can be attributed to its ability to modulate the MALAT1/miR‐129/SNCA signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Administration of resveratrol improved Parkinson’s disease‐like phenotype by suppressing apoptosis of neurons via modulating the MALAT1/miR‐129/SNCA signaling pathway

Xia

Sui

Zhang

2018

J of Cellular Biochemistry

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“…Nevertheless, the results from this study need to be taken with caution. First, most of the hemoglobin and iron related genes were identified in datasets from PD patients receiving medication and it has been documented that drug treatment can impact gene expression in blood studies (Alieva et al, 2015). In this context, amantadine, a common drug to treat PD, may cause anemia in PD patients (Foller et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Blood Transcriptomic Meta-analysis Identifies Dysregulation of Hemoglobin and Iron Metabolism in Parkinson’ Disease

Santiago

Potashkin

2017

Front. Aging Neurosci.

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Disrupted iron metabolism has been implicated in the pathogenesis of Parkinson’s disease (PD), a progressive neurodegenerative disorder that severely affects movement and coordination, yet the molecular mechanisms underlying this association remain unknown. To this end, we performed a transcriptomic meta-analysis of four blood microarrays in PD. We observed a significant downregulation of genes related to hemoglobin including, hemoglobin delta (HBD), alpha hemoglobin stabilizing protein (ASHP), genes implicated in iron metabolism including, solute carrier family 11 member 2 (SLC11A2), ferrochelatase (FECH), and erythrocyte-specific genes including erythrocyte membrane protein (EPB42), and 5′-aminolevulinate synthase 2 (ALAS2). Pathway and network analysis identified enrichment in processes related to mitochondrial membrane, oxygen transport, oxygen and heme binding, hemoglobin complex, erythrocyte development, tetrapyrrole metabolism and the spliceosome. Collectively, we identified a subnetwork of genes in blood that may provide a molecular explanation for the disrupted hemoglobin and iron metabolism in the pathogenesis of PD.

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“…The expression level of miR-7-5p is decreased in the serum of patients with PD (52). In circulating lymphocytes of treated patients, miR-7-5p and miR-9-5p are upregulated compared with untreated controls (125). Moreover, miR-22-3p is downregulated in whole blood of newly diagnosed and in treated PD patients compared with healthy controls (126), and miR-34c-3p is downregulated in brain areas of PD patients with neuropathological lesions (127).…”

Section: Inflammasome-regulating Mirnas In Human Autoimmune Diseasesmentioning

confidence: 94%

Dysregulation of Inflammasome Priming and Activation by MicroRNAs in Human Immune-Mediated Diseases

Boxberger

Hecker

Zettl

2019

The Journal of Immunology

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Inflammasomes are protein complexes that respond to a wide range of pathogens and cellular damage signals. Their activation prompts the caspase-1–mediated cleavage of the proinflammatory cytokines IL-1β and IL-18. Inflammasome dysregulation has been demonstrated to play a role in a range of diseases involving the adaptive immune system like multiple sclerosis, rheumatic diseases, and type 1 diabetes. Priming and activation of inflammasomes can be modulated by microRNAs (miRNAs), small noncoding RNAs that regulate gene expression posttranscriptionally. miRNAs, such as miR-223-3p, have been demonstrated to directly target the inflammasome components NLRP3, caspase-1, and caspase-8. Other miRNAs like miR-155-5p modulate TLR-, IL-1R–, TNFR-, and IFNAR-mediated signaling pathways upstream of the inflammasomes. In this study, we discuss how a more detailed elucidation of miRNA-driven inflammasome regulation helps in understanding the molecular processes underlying immune-mediated human diseases, holds potential for the identification of biomarkers and may offer novel targets for the development of future therapeutics.

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miRNA expression is highly sensitive to a drug therapy in Parkinson's disease

Cited by 61 publications

References 13 publications

Administration of resveratrol improved Parkinson’s disease‐like phenotype by suppressing apoptosis of neurons via modulating the MALAT1/miR‐129/SNCA signaling pathway

Administration of resveratrol improved Parkinson’s disease‐like phenotype by suppressing apoptosis of neurons via modulating the MALAT1/miR‐129/SNCA signaling pathway

Blood Transcriptomic Meta-analysis Identifies Dysregulation of Hemoglobin and Iron Metabolism in Parkinson’ Disease

Dysregulation of Inflammasome Priming and Activation by MicroRNAs in Human Immune-Mediated Diseases

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