From dysregulated microRNAs to structural alterations in the striatal region of METH-injected rats

Chavoshi, Hossein; Boroujeni, Mahdi Eskandarian; Abdollahifar, Mohammad‐Amin; Amini, Abdollah; Tehrani, Ava Modirzadeh; Moghaddam, Meysam Hassani; Norozian, Mohsen; Farahani, Reza Mastery; Aliaghaei, Abbas

doi:10.1016/j.jchemneu.2020.101854

Cited by 15 publications

(10 citation statements)

References 40 publications

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“…Recently, let-7b-5p was confirmed to serve as a potential biomarker for ischemic stroke, Parkinsonian syndromes and Alzheimer's disease ( 11 – 13 ). Importantly, let-7b-5p can facilitate neuronal degeneration and cause neurotoxicity ( 36 ). In the present study, knockdown of let-7b-5p inhibited the apoptosis of MPP + -intoxicated SH-SY5Y cells.…”

Section: Discussionmentioning

confidence: 99%

Let‑7b‑5p promotes cell apoptosis in Parkinson's disease by targeting HMGA2

et al. 2021

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Parkinson's disease (PD), a common multifactorial neurodegenerative disease, is characterized by irreversible loss of dopaminergic neurons in the substantia nigra. In-depth study of the pathogenesis of PD is of great importance. High-mobility group AT-hook 2 (HMGA2) has been proposed to be implicated with neuronal differentiation and impairment of cognitive function. However, whether HMGA2 plays a role in PD is rarely explored. In the present study, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated PD mice models and N-methyl-4- phenylpyridinium (MPP + )-treated SH-SY5Y cell models were established. Reverse transcription-quantitative PCR showed that HMGA2 displayed low levels in brain tissues of MPTP-treated mice and MPP + -treated SH-SY5Y cells. Moreover, HMGA2 overexpression suppressed SH-SY5Y cell apoptosis. Additionally, let-7b-5p bound with HMGA2 3′ untranslated region (UTR), and its expression was negatively correlated with HMGA2 level. Moreover, let-7b-5p presented high levels in brain tissues of PD mice and MPP + -treated SH-SY5Y cells, and knockdown of let-7b-5p inhibited SH-SY5Y cell apoptosis. Rescue assays illustrated that HMGA2 neutralized the promotive effects of let-7b-5p mimics on SH-SY5Y cell apoptosis. In conclusion, the present study demonstrated that let-7b-5p contributes to cell apoptosis in PD by targeting HMGA2, which offers a potential theoretical basis for the study of effective therapy in PD.

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Section: Discussionmentioning

confidence: 99%

Let‑7b‑5p promotes cell apoptosis in Parkinson's disease by targeting HMGA2

et al. 2021

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“…It is of interest that miRNA expression profiling in the DStr of METH-injected rats using high-throughput sequencing analysis identified 167 miRNAs that were dysregulated (113 up-regulated and 54 down-regulated). Using network enrichment analysis, the authors reported changes in the expression of genes that regulate PI3K-Akt and FoxO signaling [136]. In addition to changes in gene expression in the NAc and DStr, miRNA profiling is also altered in the midbrain that mainly contributes to dopaminergic signaling in MUD [137].…”

Section: Pre-clinical Studiesmentioning

confidence: 99%

Epigenetic Regulatory Dynamics in Models of Methamphetamine-Use Disorder

Jayanthi

McCoy

Cadet

2021

Genes

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Methamphetamine (METH)-use disorder (MUD) is a very serious, potentially lethal, biopsychosocial disease. Exposure to METH causes long-term changes to brain regions involved in reward processing and motivation, leading vulnerable individuals to engage in pathological drug-seeking and drug-taking behavior that can remain a lifelong struggle. It is crucial to elucidate underlying mechanisms by which exposure to METH leads to molecular neuroadaptive changes at transcriptional and translational levels. Changes in gene expression are controlled by post-translational modifications via chromatin remodeling. This review article focuses on the brain-region specific combinatorial or distinct epigenetic modifications that lead to METH-induced changes in gene expression.

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“…These effects of Ago2/miR-3068-5p happen together with the glutamate receptor, GluN1/Grin1 (Liu et al, 2021). METH induced miRNAs expressions in the striatum, damaged motor coordination, reduced striatal volume and dendritic length (Chavoshi et al, 2020). High-throughput sequencing analysis showed that miRNAs expressions were dysregulated by METH, 113 up-regulated and 54 downregulated in the DS in rats.…”

Section: Noncoding Rnas and Methamphetamine Addictionmentioning

confidence: 96%

Epigenetic mechanisms involved in methamphetamine addiction

et al. 2022

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Methamphetamine (METH) is an illicit psychostimulant that is widely abused. The molecular mechanism of METH addiction is complicated and still unknown. METH causes the release of the neurotransmitters including dopamine, glutamate, norepinephrine and serotonin, which activate various brain areas in the central nervous system. METH also induces synaptic plasticity and pathological memory enhancement. Epigenetics plays the important roles in regulating METH addiction. This review will briefly summarize the studies on epigenetics involved in METH addiction.

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From dysregulated microRNAs to structural alterations in the striatal region of METH-injected rats

Cited by 15 publications

References 40 publications

Let‑7b‑5p promotes cell apoptosis in Parkinson's disease by targeting HMGA2

Let‑7b‑5p promotes cell apoptosis in Parkinson's disease by targeting HMGA2

Epigenetic Regulatory Dynamics in Models of Methamphetamine-Use Disorder

Epigenetic mechanisms involved in methamphetamine addiction

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