Screening of microRNAs associated with Alzheimer's disease using oxidative stress cell model and different strains of senescence accelerated mice

Zhang, Rui; Zhang, Qingfu; Niu, Jingya; Lu, Kang; Xie, Bing; Cui, Dongsheng; Xu, Shunjiang

doi:10.1016/j.jns.2013.12.017

Cited by 67 publications

(49 citation statements)

References 45 publications

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“…In a mouse model with oxidative liver injury induced by treatment with the anti-tuberclosis drug isoniazid, expression of miR-122 in tissue was significantly changed at days 3 and 5 (Wu et al, 2015). In a study of miRNAs expressed in oxidatively stressed hippocampal neurons in senescence accelerated mice, miR-329, miR-193b, miR-20a, miR-296, and miR-130b were found to be upregulated (Zhang et al, 2014). These miRNAs may be involved in a variety of processes, such as regulation of cell growth, apoptosis, signal transmission, and cancer development, especially through the mitogen-activated protein kinase signaling pathway.…”

Section: Mirna Synthesis/actionmentioning

confidence: 99%

Are microRNAs true sensors of ageing and cellular senescence?

Williams

Smith

Kumar

et al. 2017

Ageing Research Reviews

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All living beings are programmed to death due to aging and age-related processes. Aging is a normal process of every living species. While all cells are inevitably progressing towards death, many disease processes accelerate the aging process, leading to senescence. Pathologies such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington’s disease, cardiovascular disease, cancer, and skin diseases have been associated with deregulated aging. Healthy aging can delay onset of all age-related diseases. Genetics and epigenetics are reported to play large roles in accelerating and/or delaying the onset of age-related diseases. Cellular mechanisms of aging and age-related diseases are not completely understood. However, recent molecular biology discoveries have revealed that microRNAs (miRNAs) are potential sensors of aging and cellular senescence. Due to miRNAs capability to bind to the 3’ untranslated region (UTR) of mRNA of specific genes, miRNAs can prevent the translation of specific genes. The purpose of our article is to highlight recent advancements in miRNAs and their involvement in cellular changes in aging and senescence. Our article discusses the current understanding of cellular senescence, its interplay with miRNAs regulation, and how they both contribute to disease processes.

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Section: Mirna Synthesis/actionmentioning

confidence: 99%

Are microRNAs true sensors of ageing and cellular senescence?

Williams

Smith

Kumar

et al. 2017

Ageing Research Reviews

View full text Add to dashboard Cite

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“…ssRNAs presumably also carry a signal encoded within the sequence of their RNA which may be transmitted via a unique molecular shape, molecular topology, and/or RNA charge density across the entire molecule. Intriguingly miRNAs enriched in certain foods may pass horizontally between species, carrying genetic regulatory information well outside of the cells in which they were initially generated (Alexandrov et al, 2012; Sarkies and Miska, 2013; Zhang et al, 2013). …”

Section: Micrornas (Mirnas)mentioning

confidence: 99%

Comparing miRNAs and viroids; highly conserved molecular mechanisms for the transmission of genetic information

Hill

Lukiw

2014

Front. Cell. Neurosci.

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“…It is known that both inflammation and oxidative stress contribute to the development of various neuropathologies including Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS) [5, 6, 20]. As discussed by Guest et al [7] the cerebrospinal fluid (CSF) of participants aged over 45 years contained statistically higher amounts of the oxidative damage marker F 2 -isoprostane (F 2 -IsoPs) and the inflammatory cytokine IL-6.…”

Section: Introductionmentioning

confidence: 99%

Isoprostanes and Neuroprostanes as Biomarkers of Oxidative Stress in Neurodegenerative Diseases

Miller

Morel

Saso

et al. 2014

Oxidative Medicine and Cellular Longevity

115

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Accumulating data shows that oxidative stress plays a crucial role in neurodegenerative disorders. The literature data indicate that in vivo or postmortem cerebrospinal fluid and brain tissue levels of F2-isoprostanes (F2-IsoPs) especially F4-neuroprotanes (F4-NPs) are significantly increased in some neurodegenerative diseases: multiple sclerosis, Alzheimer's disease, Huntington's disease, and Creutzfeldt-Jakob disease. Central nervous system is the most metabolically active organ of the body characterized by high requirement for oxygen and relatively low antioxidative activity, what makes neurons and glia highly susceptible to destruction by reactive oxygen/nitrogen species and neurodegeneration. The discovery of F2-IsoPs and F4-NPs as markers of lipid peroxidation caused by the free radicals has opened up new areas of investigation regarding the role of oxidative stress in the pathogenesis of human neurodegenerative diseases. This review focuses on the relationship between F2-IsoPs and F4-NPs as biomarkers of oxidative stress and neurodegenerative diseases. We summarize the knowledge of these novel biomarkers of oxidative stress and the advantages of monitoring their formation to better define the involvement of oxidative stress in neurological diseases.

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Screening of microRNAs associated with Alzheimer's disease using oxidative stress cell model and different strains of senescence accelerated mice

Cited by 67 publications

References 45 publications

Are microRNAs true sensors of ageing and cellular senescence?

Are microRNAs true sensors of ageing and cellular senescence?

Comparing miRNAs and viroids; highly conserved molecular mechanisms for the transmission of genetic information

Isoprostanes and Neuroprostanes as Biomarkers of Oxidative Stress in Neurodegenerative Diseases

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