miR-196a Ameliorates Cytotoxicity and Cellular Phenotype in Transgenic Huntington’s Disease Monkey Neural Cells

Kunkanjanawan, Tanut; Carter, Richard L.; Prucha, Melinda S.; Yang, Jingyuan; Parnpai, Rangsun; Chan, Anthony W.S.

doi:10.1371/journal.pone.0162788

Cited by 33 publications

(22 citation statements)

References 74 publications

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“…In case of neurodegeneration, oxidative stress dependent neurotoxicity and apoptosis was linked with following microRNAs: miR-98 , miR-132 , miR-153 , miR-200a , miR-186 , miR-221 , miR-196a , miR-22 , miR-107 , miR-223 , miR-320 , miR-125b , miR-181 , miR-365 , miR-193 , miR-49 , miR-378 , miR-25 , miR-30d-5p , miR-26b , miR-592-5p , miR-153 , miR-155 , miR-212 , miR-183/96/182 cluster, miR-146a [94,151,153,154,155,156,157,158,159,160,161,162,163,164,165,166,167,168,169,170,171,172,173,174,175,176,177,178,179,180,181,182,183,184,185,186]. MicroRNAs that are linked to the therapy resistance and sensitivity are the ones engaged in cancer cell survival.…”

Section: More About Microrna In Neuropathologymentioning

confidence: 99%

MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer

Godlewski

Lenart

Salińska

2019

ncRNA

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The mammalian brain is made up of billions of neurons and supporting cells (glial cells), intricately connected. Molecular perturbations often lead to neurodegeneration by progressive loss of structure and malfunction of neurons, including their death. On the other side, a combination of genetic and cellular factors in glial cells, and less frequently in neurons, drive oncogenic transformation. In both situations, microenvironmental niches influence the progression of diseases and therapeutic responses. Dynamic changes that occur in cellular transcriptomes during the progression of developmental lineages and pathogenesis are controlled through a variety of regulatory networks. These include epigenetic modifications, signaling pathways, and transcriptional and post-transcriptional mechanisms. One prominent component of the latter is small non-coding RNAs, including microRNAs, that control the vast majority of these networks including genes regulating neural stemness, differentiation, apoptosis, projection fates, migration and many others. These cellular processes are also profoundly dependent on the microenvironment, stemness niche, hypoxic microenvironment, and interactions with associated cells including endothelial and immune cells. Significantly, the brain of all other mammalian organs expresses the highest number of microRNAs, with an additional gain in expression in the early stage of neurodegeneration and loss in expression in oncogenesis. However, a mechanistic explanation of the concept of an apparent inverse correlation between the odds of cancer and neurodegenerative diseases is only weakly developed. In this review, we thus will discuss widespread de-regulation of microRNAome observed in these two major groups of brain pathologies. The deciphering of these intricacies is of importance, as therapeutic restoration of pre-pathological microRNA landscape in neurodegeneration must not lead to oncogenesis and vice versa. We thus focus on microRNAs engaged in cellular processes that are inversely regulated in these diseases. We also aim to define the difference in microRNA networks between pro-survival and pro-apoptotic signaling in the brain.

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Section: More About Microrna In Neuropathologymentioning

confidence: 99%

MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer

Godlewski

Lenart

Salińska

2019

ncRNA

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“…In the striatum of HD brains, reduced mitochondrial function is evidenced by low oxidative phosphorylation and high oxidative stress. Interestingly, miR-196a upregulation modulates mitochondrial function by its effects on CBP and PGC-1α, and targeting miR-196a was reported to restore mitochondrial function in HD [46]. Furthermore, miR-196a also targets the 3′UTR of RAN binding protein 10 (RANBP10), an action which enhances neuronal morphogenesis and intracellular transport in an HD mouse model [47].…”

Section: Ncrnas In Other Mechanisms Of Hd Pathogenesismentioning

confidence: 99%

“…HD brain, striatum [46] miR-196a up The higher expression of RAN binding protein 10 (RANBP10) in the brains of HD transgenic mice and exacerbates neuronal morphology and intracellular transport. miR-196a suppress the expression of RANBP10 through binding to its 3'UTR.…”

Section: Ncrnas In Other Mechanisms Of Hd Pathogenesismentioning

confidence: 99%

Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases

2020

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Recent transcriptome analyses have revealed that noncoding RNAs (ncRNAs) are broadly expressed in mammalian cells and abundant in the CNS, with tissue and cell type-specific expression patterns. Moreover, ncRNAs have been found to intricately and dynamically regulate various signaling pathways in neurodegeneration. As such, some antisense transcripts and microRNAs are known to directly affect neurodegeneration in disease contexts. The functions of ncRNAs in pathogenesis are unique for each disorder, as are the pertinent networks of ncRNA/miRNA/ mRNA that mediate these functions. Thus, further understanding of ncRNA biogenesis and effects might aid the discovery of diagnostic biomarkers or development of effective therapeutics for neurodegenerative disorders. Here, we review the ncRNAs that have so far been identified in major neurodegenerative disease etiology and the mechanisms that link ncRNAs with disease-specific phenotypes, such as HTT aggregation in HD, α-synuclein in PD, and Aβ plaques and hyperphosphorylated Tau in AD. We also summarize the known lncRNA/miRNA/mRNA networks that participate in neurodegenerative diseases, and we discuss ncRNA-related treatments shown to delay disease onset and prolong lifespan in rodent models.

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“…Similar results were reported by another group ( Im et al, 2013 ). Cytotoxicity and apoptosis are ameliorated by overexpressing miR-196a through upregulation of CBP and PGC-1α in HD monkey neural progenitor cells ( Kunkanjanawan et al, 2016 ).…”

Section: Huntington’s Diseasementioning

confidence: 99%

Transcriptional Dysregulation and Post-translational Modifications in Polyglutamine Diseases: From Pathogenesis to Potential Therapeutic Strategies

Xiang

Zhang

Dong

et al. 2018

Front. Mol. Neurosci.

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Polyglutamine (polyQ) diseases are hereditary neurodegenerative disorders caused by an abnormal expansion of a trinucleotide CAG repeat in the coding region of their respective associated genes. PolyQ diseases mainly display progressive degeneration of the brain and spinal cord. Nine polyQ diseases are known, including Huntington’s disease (HD), spinal and bulbar muscular atrophy (SBMA), dentatorubral-pallidoluysian atrophy (DRPLA), and six forms of spinocerebellar ataxia (SCA). HD is the best characterized polyQ disease. Many studies have reported that transcriptional dysregulation and post-translational disruptions, which may interact with each other, are central features of polyQ diseases. Post-translational modifications, such as the acetylation of histones, are closely associated with the regulation of the transcriptional activity. A number of groups have studied the interactions between the polyQ proteins and transcription factors. Pharmacological drugs or genetic manipulations aimed at correcting the dysregulation have been confirmed to be effective in the treatment of polyQ diseases in many animal and cellular models. For example, histone deaceylase inhibitors have been demonstrated to have beneficial effects in cases of HD, SBMA, DRPLA, and SCA3. In this review, we describe the transcriptional and post-translational dysregulation in polyQ diseases with special focus on HD, and we summarize and comment on potential treatment approaches targeting disruption of transcription and post-translation processes in these diseases.

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miR-196a Ameliorates Cytotoxicity and Cellular Phenotype in Transgenic Huntington’s Disease Monkey Neural Cells

Cited by 33 publications

References 74 publications

MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer

MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer

Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases

Transcriptional Dysregulation and Post-translational Modifications in Polyglutamine Diseases: From Pathogenesis to Potential Therapeutic Strategies

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