Novel BDNF-regulatory microRNAs in neurodegenerative disorders pathogenesis: An in silico study

Khani-Habibabadi, Fatemeh; Askari, Shahrzad; Zahiri, Javad; Javan, Mohammad; Behmanesh, Mehrdad

doi:10.1016/j.compbiolchem.2019.107153

Cited by 16 publications

(9 citation statements)

References 87 publications

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“…A number of recent studies, obtained from high throughput sequencing screening of different brain regions or from neurological disorders, have identified seven miRNAs (miR-15a, miR-206, miR-155-5p, miR-16, miR-103-3p, miR-330-3p, Let-7a-3p) correlated with BDNF [ 55 ]. Previous data published by Schratt et al reported the involvement of miR-134 in BDNF-regulated dendritic spine size in hippocampal neurons.…”

Section: The Human Bdnf Gene: Transcripts and Variantsmentioning

confidence: 99%

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Colucci-D’Amato

Speranza

Volpicelli

2020

IJMS

522

249

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Brain-derived neurotrophic factor (BDNF) is one of the most distributed and extensively studied neurotrophins in the mammalian brain. BDNF signals through the tropomycin receptor kinase B (TrkB) and the low affinity p75 neurotrophin receptor (p75NTR). BDNF plays an important role in proper growth, development, and plasticity of glutamatergic and GABAergic synapses and through modulation of neuronal differentiation, it influences serotonergic and dopaminergic neurotransmission. BDNF acts as paracrine and autocrine factor, on both pre-synaptic and post-synaptic target sites. It is crucial in the transformation of synaptic activity into long-term synaptic memories. BDNF is considered an instructive mediator of functional and structural plasticity in the central nervous system (CNS), influencing dendritic spines and, at least in the hippocampus, the adult neurogenesis. Changes in the rate of adult neurogenesis and in spine density can influence several forms of learning and memory and can contribute to depression-like behaviors. The possible roles of BDNF in neuronal plasticity highlighted in this review focus on the effect of antidepressant therapies on BDNF-mediated plasticity. Moreover, we will review data that illustrate the role of BDNF as a potent protective factor that is able to confer protection against neurodegeneration, in particular in Alzheimer’s disease. Finally, we will give evidence of how the involvement of BDNF in the pathogenesis of brain glioblastoma has emerged, thus opening new avenues for the treatment of this deadly cancer.

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Section: The Human Bdnf Gene: Transcripts and Variantsmentioning

confidence: 99%

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Colucci-D’Amato

Speranza

Volpicelli

2020

IJMS

522

249

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“…miRNA can lead to silencing of its target mRNA either via inhibition of translation or degradation of the mRNA 13,15 . Furthermore, miRNAs were reported as important regulators in many biological processes including cell proliferation, differentiation, development, metabolism and so on 16 .Recent studies had shown the essential roles of miRNAs in regulation in diverse neurological and neurodegenerative disorders, such as Parkinson's disease, Huntington's disease [17][18][19] . The altered miRNA expression and the potential role on the altered mRNA expression have been reported in cellular model of mice and human HD samples with microarray technologies and next generation sequencing 20 .…”

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confidence: 99%

“…Recent studies had shown the essential roles of miRNAs in regulation in diverse neurological and neurodegenerative disorders, such as Parkinson's disease, Huntington's disease [17][18][19] . The altered miRNA expression and the potential role on the altered mRNA expression have been reported in cellular model of mice and human HD samples with microarray technologies and next generation sequencing 20 .…”

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confidence: 99%

MicroRNA editing patterns in Huntington’s disease

Guo

Yang

Jiang

et al. 2022

Sci Rep

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Huntington’s disease (HD) is a neurodegenerative disease. MicroRNAs (miRNAs) are small non-coding RNAs that mediate post-transcriptional regulation of target genes. Although miRNAs are extensively edited in human brains, the editome of miRNAs in brains of HD patients is largely unknown. By analyzing the small RNA sequencing profiles of brain tissues of 28 HD patients and 83 normal controls, 1182 miRNA editing sites with significant editing levels were identified. In addition to 27 A-to-I editing sites, we identified 3 conserved C-to-U editing sites in miRNAs of HD patients. 30 SNPs in the miRNAs of HD patients were also identified. Furthermore, 129 miRNA editing events demonstrated significantly different editing levels in prefrontal cortex samples of HD patients (HD-PC) when compared to those of healthy controls. We found that hsa-mir-10b-5p was edited to have an additional cytosine at 5’-end in HD-PC, and the edited hsa-mir-10b repressed GTPBP10 that was often downregulated in HD. The down-regulation of GTPBP10 might contribute to the progression of HD by causing gradual loss of function of mitochondrial. These results provide the first endeavor to characterize the miRNA editing events in HD and their potential functions.

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“…Previous studies have provided data that can support the possible interaction of HOTAIR and MALAT1 with BDNF regulation via the ceRNA mechanism. Also, the ceRNA hypothesis explains why a significant positive correlation between MALAT1 and HOTAIR lncRNAs may exist (Tian et al 2014;Khani-Habibabadi et al 2019, Q. Li et al 2018Chang et al 2018) However, the cause of this positive correlation between HOTAIR and MALAT1 needs further study.…”

Section: Discussionmentioning

confidence: 99%

Fingolimod Regulates BDNF-AS and HOTAIR Expression in Multiple Sclerosis Patients

Khani-Habibabadi

Sahraian

Javan

et al. 2021

Preprint

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Objective: Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, is expressed by neurons and glial cells in the central nervous system (CNS). In the CNS, BDNF is responsible for neuroprotection and neurogenesis. Recent studies showed that the Fingolimod, the first oral medicine for relapsing-remitting multiple sclerosis (RR-MS), induces BDNF expression. Besides, It is well demonstrated that long noncoding RNAs (lncRNAs) have a pivotal role in gene regulation. This study is mainly focused on how Fingolimod treatment plays role in BDNF regulation in coordination with lncRNAs. Methods: An in-silico study was performed to predict BDNF-regulatory candidate lncRNAs using online tools. Then, the expression of BDNF-related lncRNAs was analyzed in patients with relapsing-remitting multiple sclerosis (RRMS) at baseline and after three months of Fingolimod treatment. Results: Based on in silico results, two lncRNAs with potential regulatory functions on the BDNF including, Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) and HOX Transcript Antisense RNA (HOTAIR), and also natural antisense of BDNF were selected. Fingolimod treatment increased the expression of HOTAIR lncRNA; however, the BDNF antisense RNA (BDNF-AS) expression was reduced dramatically. Furthermore, the results indicate a positive correlation between HOTAIR and MALAT1 lncRNAs and BDNF. Also, after Fingolimod treatment, the patients' EDSS scores were declined or remained unchanged, indicating disease hindrance by Fingolimod therapy. Conclusion: Altogether, fingolimod exerts protective roles in RRMS patients probably by the mediation of HOTIAR and BDNF-AS lncRNAs.

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Novel BDNF-regulatory microRNAs in neurodegenerative disorders pathogenesis: An in silico study

Cited by 16 publications

References 87 publications

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

MicroRNA editing patterns in Huntington’s disease

Fingolimod Regulates BDNF-AS and HOTAIR Expression in Multiple Sclerosis Patients

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