Abstract:A general hallmark of neurological diseases is the loss of redox homeostasis that triggers oxidative damages to biomolecules compromising neuronal function. Under physiological conditions the steady-state concentrations of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are finely regulated for proper cellular functions. Reduced surveillance of endogenous antioxidant defenses and/or increased ROS/RNS production leads to oxidative stress with consequent alteration of physiological processes. N… Show more
“…miRNAs are involved in the regulation of intracellular redox and post-transcriptional regulation of key components of the ROS/ reactive nitrogen (RNS) pathway, including Nrf2. 9 Jing Zhou et al 10 showed that H 2 O 2 activated the Nrf2 signalling pathway in a mouse corneal epithelial progenitor cell line (TKE2) and increased the expression of miR-125b.…”
Section: Mir-125b Belongsmentioning
confidence: 99%
“…Recent studies have shown that miRNAs regulate Nrf2 directly or indirectly, which may be an important mechanism underlying miRNAs involvement in cell differentiation and apoptosis. miRNAs are involved in the regulation of intracellular redox and post‐transcriptional regulation of key components of the ROS/reactive nitrogen (RNS) pathway, including Nrf2 . Jing Zhou et al showed that H 2 O 2 activated the Nrf2 signalling pathway in a mouse corneal epithelial progenitor cell line (TKE2) and increased the expression of miR‐125b.…”
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that affects the quality of life of infants. At present, premature exposure to hyperoxia for extended periods of time is believed to affect the development of lung tissue and vascularity, resulting in BPD. The oxidative stress caused by hyperoxia exposure is an important risk factor for BPD in premature infants. Nuclear factor E2‐related factor 2 (Nrf2) is an important regulator of antioxidant mechanisms. As a microRNA, microRNA‐125b (miR‐125b) plays an important role in cell proliferation, differentiation and apoptosis. Although the Nrf2/ARE pathway has been extensively studied, little is known about the regulatory role of microRNAs in Nrf2 expression. In this study, the expression levels of Nrf2 and miR‐125b in the lung tissues of premature Sprague Dawley (SD) rats and A549 cells exposed to hyperoxia were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR), and the apoptosis of A549 cells was detected by flow cytometry. The results showed that Nrf2 and miRNA‐125b in the lung tissues of premature rats increased significantly upon exposure to hyperoxia and played a protective role. Nrf2 was suppressed by small interfering RNA (siRNA) in A549 cells, miR‐125b was similarly inhibited, and apoptosis was significantly increased. These results suggest that miR‐125b helps protect against BPD as a downstream target of Nrf2.
“…miRNAs are involved in the regulation of intracellular redox and post-transcriptional regulation of key components of the ROS/ reactive nitrogen (RNS) pathway, including Nrf2. 9 Jing Zhou et al 10 showed that H 2 O 2 activated the Nrf2 signalling pathway in a mouse corneal epithelial progenitor cell line (TKE2) and increased the expression of miR-125b.…”
Section: Mir-125b Belongsmentioning
confidence: 99%
“…Recent studies have shown that miRNAs regulate Nrf2 directly or indirectly, which may be an important mechanism underlying miRNAs involvement in cell differentiation and apoptosis. miRNAs are involved in the regulation of intracellular redox and post‐transcriptional regulation of key components of the ROS/reactive nitrogen (RNS) pathway, including Nrf2 . Jing Zhou et al showed that H 2 O 2 activated the Nrf2 signalling pathway in a mouse corneal epithelial progenitor cell line (TKE2) and increased the expression of miR‐125b.…”
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that affects the quality of life of infants. At present, premature exposure to hyperoxia for extended periods of time is believed to affect the development of lung tissue and vascularity, resulting in BPD. The oxidative stress caused by hyperoxia exposure is an important risk factor for BPD in premature infants. Nuclear factor E2‐related factor 2 (Nrf2) is an important regulator of antioxidant mechanisms. As a microRNA, microRNA‐125b (miR‐125b) plays an important role in cell proliferation, differentiation and apoptosis. Although the Nrf2/ARE pathway has been extensively studied, little is known about the regulatory role of microRNAs in Nrf2 expression. In this study, the expression levels of Nrf2 and miR‐125b in the lung tissues of premature Sprague Dawley (SD) rats and A549 cells exposed to hyperoxia were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR), and the apoptosis of A549 cells was detected by flow cytometry. The results showed that Nrf2 and miRNA‐125b in the lung tissues of premature rats increased significantly upon exposure to hyperoxia and played a protective role. Nrf2 was suppressed by small interfering RNA (siRNA) in A549 cells, miR‐125b was similarly inhibited, and apoptosis was significantly increased. These results suggest that miR‐125b helps protect against BPD as a downstream target of Nrf2.
“…Nrf2, involved in redox reactions, participates in ER stress-induced apoptosis and together with ATF4 repress miR-106b-25 cluster. It has been shown that the Nrf2/ATF4/miR-106b-25 cluster may be relevant for ALS pathogenesis [244]. In addition, miR-142-5p, that is downregulated in the CSF of ALS patients, has been shown to reduce OS via the upregulation of the Nrf2 signaling pathway [236,245].…”
Oxidative stress (OS) results from an imbalance between the production of reactive oxygen species and the cellular antioxidant capacity. OS plays a central role in neurodegenerative diseases, where the progressive accumulation of reactive oxygen species induces mitochondrial dysfunction, protein aggregation and inflammation. Regulatory non-protein-coding RNAs (ncRNAs) are essential transcriptional and post-transcriptional gene expression controllers, showing a highly regulated expression in space (cell types), time (developmental and ageing processes) and response to specific stimuli. These dynamic changes shape signaling pathways that are critical for the developmental processes of the nervous system and brain cell homeostasis. Diverse classes of ncRNAs have been involved in the cell response to OS and have been targeted in therapeutic designs. The perturbed expression of ncRNAs has been shown in human neurodegenerative diseases, with these changes contributing to pathogenic mechanisms, including OS and associated toxicity. In the present review, we summarize existing literature linking OS, neurodegeneration and ncRNA function. We provide evidences for the central role of OS in age-related neurodegenerative conditions, recapitulating the main types of regulatory ncRNAs with roles in the normal function of the nervous system and summarizing up-to-date information on ncRNA deregulation with a direct impact on OS associated with major neurodegenerative conditions.
“…In fact, the DNA damage from ionizing radiation has thus been attributed to the formation of radicals from the radiolysis of water molecules, as will be treated extensively in a later paragraph. More recently, also in light of the progress on understanding radicals as elements of intracellular and intercellular communication (Paladino et al, 2018), more and more weight is being given to biological pathways mediated by mitochondrial oxide-reduction while intermediate metabolic products can lead to oxidation, nitrosylation, and alkylation of DNA (Hekimi et al, 2011). Whatever their origin, ROS are able to induce DNA damage either directly or indirectly by interfering with the activity of the epigenetic regulatory factors and the DDR proteins.…”
Section: Aging: Definition and Characteristicsmentioning
The increasing duration of space missions involves a progressively higher exposure of astronauts to cosmic rays, whose most hazardous component is made up of High-Atomic number and High-Energy (HZE) ions. HZE ions interact along their tracks with biological molecules inducing changes on living material qualitatively different from that observed after irradiation for therapeutic purposes or following nuclear accidents. HZE ions trigger in cells different responses initialized by DNA damage and mitochondria dysregulation, which cause a prolonged state of sterile inflammation in the tissues. These cellular phenomena may explain why spending time in space was found to cause the onset of a series of diseases normally related to aging. These changes that mimic aging but take place more quickly make space flights also an opportunity to study the mechanisms underlying aging. In this short review, we describe the biological mechanisms underlying cell senescence and aging; the peculiar characteristics of HZE ions, their interaction with living matter and the effects on the organism; the key role of mitochondria in HZE ion-induced health effects and aging-related phenomena.
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