scholarly journals The Role of Exosomal microRNAs and Oxidative Stress in Neurodegenerative Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Xiaoyu Wang ◽  
Yunxiang Zhou ◽  
Qiannan Gao ◽  
Dongnan Ping ◽  
Yali Wang ◽  
...  

Neurodegenerative diseases including Alzheimer’s disease and Parkinson’s disease are aging-associated diseases with irreversible damage of brain tissue. Oxidative stress is commonly detected in neurodegenerative diseases and related to neuronal injury and pathological progress. Exosome, one of the extracellular vesicles, is demonstrated to carry microRNAs (miRNAs) and build up a cell-cell communication in neurons. Recent research has found that exosomal miRNAs regulate the activity of multiple physiological pathways, including the oxidative stress response, in neurodegenerative diseases. Here, we review the role of exosomal miRNAs and oxidative stress in neurodegenerative diseases. Firstly, we explore the relationship between oxidative stress and neurodegenerative diseases. Secondly, we introduce the characteristics of exosomes and roles of exosome-related miRNAs. Thirdly, we summarized the crosstalk between exosomal miRNAs and oxidative stress in neurodegenerative diseases. Fourthly, we discuss the potential of exosomes to be a biomarker in neurodegenerative diseases. Finally, we summarize the advantages of exosome-based delivery and present situation of research on exosome-based delivery of therapeutic miRNA. Our work is aimed at probing and reinforcing the recognition of the pathomechanism of neurodegenerative diseases and providing the basis for novel strategies of clinical diagnosis and treatment.

2019 ◽  
Vol 7 (3) ◽  
pp. 116-128
Author(s):  
Jianyang Liu ◽  
Jialin He ◽  
Yan Huang ◽  
Han Xiao ◽  
Zheng Jiang ◽  
...  

The central role of the Golgi apparatus in critical cellular processes such as the transport, processing, and sorting of proteins and lipids has placed it at the forefront of cell science. Golgi apparatus dysfunction caused by primary defects within the Golgi or pharmacological and oxidative stress has been implicated in a wide range of neurodegenerative diseases. In addition to participating in disease progression, the Golgi apparatus plays pivotal roles in angiogenesis, neurogenesis, and synaptogenesis, thereby promoting neurological recovery. In this review, we focus on the functions of the Golgi apparatus and its mediated events during neurorestoration.


Author(s):  
Linlin Zhang ◽  
Aurelio Reyes ◽  
Xiangdong Wang

Abstract: The discovery of charged molecules being able to cross the mitochondrial membrane has prompted many scholars to exploit this idea to find a way of preventing or slowing down aging. In this paper, we will focus on mitochondriatargeted antioxidants, which are cationic derivatives of plastoquinone, and in particular on the mitochondria-targeted antioxidant therapy of neurodegenerative diseases. It is well known that the accumulation of amyloid-β peptide (Aβ) in mitochondria and its related mitochondrial dysfunction are critical signatures of Alzheimer’ s disease (AD). In another neurodegenerative disease, Parkinson’s disease (PD), the loss of dopaminergic neurons in the substantia nigra and the production of Lewy bodies are among their pathological features. Pathogenesis of Parkinson’s disease and Alzheimer’s disease has been frequently linked to mitochondrial dysfunction and oxidative stress. Recent studies show that MitoQ, a mitochondria-targeted antioxidant, may possess therapeutic potential for Aβ-related and oxidative stress-associated neurodegenerative diseases, especially AD. Although MitoQ has been developed to the stage of clinical trials in PD, its true clinical effect still need further verification. This review aims to discuss the role of mitochondrial pathology in neurodegenerative diseases, as well as the recent development of mitochondrial targeted antioxidants as a potential treatment for these diseases by removing excess oxygen free radicals and inhibiting lipid peroxidation in order to improve mitochondrial function.  


2020 ◽  
Vol 21 (10) ◽  
pp. 3653
Author(s):  
Sara Cheleschi ◽  
Marcella Barbarino ◽  
Ines Gallo ◽  
Sara Tenti ◽  
Maria Bottaro ◽  
...  

Hydrostatic pressure (HP) modulates chondrocytes metabolism, however, its ability to regulate oxidative stress and microRNAs (miRNA) has not been clarified. The aim of this study was to investigate the role of miR-34a, miR-146a, and miR-181a as possible mediators of HP effects on oxidative stress in human osteoarthritis (OA) chondrocytes. Chondrocytes were exposed to cyclic low HP (1–5 MPa) and continuous static HP (10 MPa) for 3~h. Metalloproteinases (MMPs), disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5, type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma 2 (BCL2) were evaluated by quantitative real-time polymerase chain reaction qRT-PCR, apoptosis and reactive oxygen species ROS production by cytometry, and β-catenin by immunofluorescence. The relationship among HP, the studied miRNA, and oxidative stress was assessed by transfection with miRNA specific inhibitors. Low cyclical HP significantly reduced apoptosis, the gene expression of MMP-13, ADAMTS5, miRNA, the production of superoxide anion, and mRNA levels of antioxidant enzymes. Conversely, an increased Col2a1 and BCL2 genes was observed. β-catenin protein expression was reduced in cells exposed to HP 1–5 MPa. Opposite results were obtained following continuous static HP application. Finally, miRNA silencing enhanced low HP and suppressed continuous HP-induced effects. Our data suggest miRNA as one of the mechanisms by which HP regulates chondrocyte metabolism and oxidative stress, via Wnt/β-catenin pathway.


Author(s):  
Sara Rahsepar ◽  
Amirhooshang Mohammadpour

Bipolar disorder is a chronic psychological condition that disturbs many patients' lives around the world. The exact pathophysiology of bipolar disorder is yet unknown, but there are several hypotheses to explain this condition. One of the most challenging theories is the role of oxidative stress in the progression of bipolar disorder. Here, we conducted a narrative review to gather the studies that investigated the relationship between bipolar disorder and oxidative stress. We searched PubMed, Scopus, Web of science, and google scholar databases using the following keywords: “bipolar disorder,” “oxidative stress,” “oxidative markers,” and “bipolar patients.”     A majority of studies showed that oxidative markers such as Thiobarbituric acid reactive substances are significantly higher in bipolar patients compared to healthy subjects. Based on the included articles, bipolar disorder is associated with oxidative stress. Nevertheless, further well-established Cohorts are required to support these results.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Sara Manti ◽  
Lucia Marseglia ◽  
Gabriella D’Angelo ◽  
Caterina Cuppari ◽  
Erika Cusumano ◽  
...  

Although extensive epidemiological and laboratory studies have been performed to identify the environmental and immunological causes of atopy, genetic predisposition seems to be the biggest risk factor for allergic diseases. The onset of atopic diseases may be the result of heritable changes of gene expression, without any alteration in DNA sequences occurring in response to early environmental stimuli. Findings suggest that the establishment of a peculiar epigenetic pattern may also be generated by oxidative stress (OS) and perpetuated by the activation of OS-related genes. Analyzing the role of maternal and neonatal oxidative stress and oxidative stress-inducible genes, the purpose of this review was to summarize what is known about the relationship between maternal and neonatal OS-related genes and the development of atopic diseases.


Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 314 ◽  
Author(s):  
Alexandre Vallée ◽  
Yves Lecarpentier ◽  
Rémy Guillevin ◽  
Jean-Noël Vallée

Parkinson’s disease (PD) is one of the main neurodegenerative disease characterized by a progressive degeneration of neurons constituted by dopamine in the substantia nigra pars compacta. The etiologies of PD remain unclear. Aging is the main risk factor for PD. Aging could dysregulate molecular pathways controlling cell homeostatic mechanisms. PD cells are the sites of several metabolic abnormalities including neuroinflammation and oxidative stress. Metabolic structures are driven by circadian rhythms. Biologic rhythms are complex systems interacting with the environment and controlling several physiological pathways. Recent findings have shown that the dysregulation of the circadian rhythms is correlated with PD and its metabolic dysregulations. This review is focused on the key role of circadian rhythms and their impact on neuroinflammation and oxidative stress in Parkinson’s disease.


2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Jun Lu ◽  
Yan Zhang ◽  
Jinqi Liang ◽  
Jiayu Diao ◽  
Peilong Liu ◽  
...  

Osteoporosis (OP) is an aging-related disease involving permanent bone tissue atrophy. Most patients with OP show high levels of oxidative stress (OS), which destroys the microstructure of bone tissue and promotes disease progression. Exosomes (exos) help in the delivery of microRNAs (miRNAs) and allow intercellular communication. In OP, exosomal miRNAs modulate several physiological processes, including the OS response. In the present review, we aim to describe how exosomal miRNAs and OS contribute to OP. We first summarize the relationship of OS with OP and then detail the features of exos along with the functions of exo-related miRNAs. Further, we explore the interplay between exosomal miRNAs and OS in OP and summarize the functional role of exos in OP. Finally, we identify the advantages of exo-based miRNA delivery in treatment strategies for OP. Our review seeks to improve the current understanding of the mechanism underlying OP pathogenesis and lay the foundation for the development of novel theranostic approaches for OP.


2019 ◽  
Vol 20 (23) ◽  
pp. 6055 ◽  
Author(s):  
Konovalova ◽  
Gerasymchuk ◽  
Parkkinen ◽  
Chmielarz ◽  
Domanskyi

MicroRNAs are post-transcriptional regulators of gene expression, crucial for neuronal differentiation, survival, and activity. Age-related dysregulation of microRNA biogenesis increases neuronal vulnerability to cellular stress and may contribute to the development and progression of neurodegenerative diseases. All major neurodegenerative disorders are also associated with oxidative stress, which is widely recognized as a potential target for protective therapies. Albeit often considered separately, microRNA networks and oxidative stress are inextricably entwined in neurodegenerative processes. Oxidative stress affects expression levels of multiple microRNAs and, conversely, microRNAs regulate many genes involved in an oxidative stress response. Both oxidative stress and microRNA regulatory networks also influence other processes linked to neurodegeneration, such as mitochondrial dysfunction, deregulation of proteostasis, and increased neuroinflammation, which ultimately lead to neuronal death. Modulating the levels of a relatively small number of microRNAs may therefore alleviate pathological oxidative damage and have neuroprotective activity. Here, we review the role of individual microRNAs in oxidative stress and related pathways in four neurodegenerative conditions: Alzheimer’s (AD), Parkinson’s (PD), Huntington’s (HD) disease, and amyotrophic lateral sclerosis (ALS). We also discuss the problems associated with the use of oversimplified cellular models and highlight perspectives of studying microRNA regulation and oxidative stress in human stem cell-derived neurons.


2020 ◽  
pp. 29-42
Author(s):  
S. V. Bulgakova ◽  
A. V. Melikova

Postmenopausal osteoporosis is a disease of great medical and social significance for the world population. At the same time, the underlying pathogenesis of this pathology is not fully understood. A large body of research suggests that endocrine changes associated with postmenopause can lead to disruption of redox homeostasis and oxidative stress that affects bone metabolism. This literature review analyzes the relationship between hypoestrogenemia, oxidative stress and postmenopausal osteoporosis, as well as methods for the prevention and treatment of these conditions.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Elżbieta Miller ◽  
Agnieszka Morel ◽  
Luciano Saso ◽  
Joanna Saluk

Accumulating data shows that oxidative stress plays a crucial role in neurodegenerative disorders. The literature data indicate thatin vivoor 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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