scholarly journals Therapeutic Strategies for Oxidative Stress-Related Cardiovascular Diseases: Removal of Excess Reactive Oxygen Species in Adult Stem Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hyunyun Kim ◽  
Jisoo Yun ◽  
Sang-Mo Kwon
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Stem Cell ◽  
Cardiovascular Diseases ◽  
Progenitor Cells ◽  
Adult Stem Cells ◽  
Reactive Oxygen ◽  
Therapeutic Strategies ◽  
Oxygen Species

Accumulating evidence indicates that acute and chronic uncontrolled overproduction of oxidative stress-related factors including reactive oxygen species (ROS) causes cardiovascular diseases (CVDs), atherosclerosis, and diabetes. Moreover ROS mediate various signaling pathways underlying vascular inflammation in ischemic tissues. With respect to stem cell-based therapy, several studies clearly indicate that modulating antioxidant production at cellular levels enhances stem/progenitor cell functionalities, including proliferation, long-term survival in ischemic tissues, and complete differentiation of transplanted cells into mature vascular cells. Recently emerging therapeutic strategies involving adult stem cells, including endothelial progenitor cells (EPCs), for treating ischemic CVDs have highlighted the need to control intracellular ROS production, because it critically affects the replicative senescence ofex vivoexpanded therapeutic cells. Better understanding of the complexity of cellular ROS in stem cell biology might improve cell survival in ischemic tissues and enhance the regenerative potentials of transplanted stem/progenitor cells. In this review, we will discuss the nature and sources of ROS, drug-based therapeutic strategies for scavenging ROS, and EPC based therapeutic strategies for treating oxidative stress-related CVDs. Furthermore, we will discuss whether primed EPCs pretreated with natural ROS-scavenging compounds are crucial and promising therapeutic strategies for vascular repair.

scholarly journals A reactive oxygen species-generating, cyclooxygenase-2 inhibiting, cancer stem cell-potent tetranuclear copper(ii) cluster

2017 ◽  
Vol 46 (38) ◽  
pp. 12785-12789 ◽  
Author(s):  
C. Lu ◽  
K. Laws ◽  
A. Eskandari ◽  
K. Suntharalingam
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Schiff Base ◽  
Stem Cell ◽  
Cancer Stem Cells ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Cyclooxygenase 2 ◽  
Oxygen Species

Tetranuclear copper(ii) complexes containing multiple diclofenac and Schiff base moieties,1–4, are shown to kill bulk cancer cells and cancer stem cells (CSCs) with low micromolar potency.

scholarly journals Controlled intracellular generation of reactive oxygen species in human mesenchymal stem cells using porphyrin conjugated nanoparticles

Nanoscale ◽  
2015 ◽  
Vol 7 (34) ◽  
pp. 14525-14531 ◽  
Author(s):  
Andrea S. Lavado ◽  
Veeren M. Chauhan ◽  
Amer Alhaj Zen ◽  
Francesca Giuntini ◽  
D. Rhodri E. Jones ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Visible Light ◽  
Human Mesenchymal Stem Cells ◽  
Reactive Oxygen ◽  
Cellular Communication ◽  
Oxygen Species

Newly synthesised Zn (ii) porphyrin nanoparticle conjugates were irradiated with visible light to generate controlled amounts of ROS in hMSCs to advance the study of oxidative stress and cellular communication.

scholarly journals The Role of Nrf2 and PPARγ in the Improvement of Oxidative Stress in Hypertension and Cardiovascular Diseases

2020 ◽  
pp. S541-S553
Author(s):  
I DOVINOVA ◽  
M KVANDOVA ◽  
P BALIS ◽  
L GRESOVA ◽  
M MAJZUNOVA ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Nuclear Receptor ◽  
Redox Regulation ◽  
Reactive Oxygen ◽  
Peroxisome Proliferator ◽  
Oxygen Species ◽  
Response Element ◽  
Stress Oxidative

Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological changes. Oxidative stress helps to regulate cellular phenotypes in physiological and pathological conditions. Nrf2 (nuclear factor erythroid 2-related factor 2, NFE2L2) transcription factor functions as a target nuclear receptor against oxidative stress and is a key factor in redox regulation in hypertension and cardiovascular disease. Nrf2 mediates transcriptional regulation of a variety of target genes. The Keap1-Nrf2-ARE system regulates many detoxification and antioxidant enzymes in cells after the exposure to reactive oxygen species and electrophiles. Activation of Nrf2/ARE signaling is differentially regulated during acute and chronic stress. Keap1 normally maintains Nrf2 in the cytosol and stimulates its degradation through ubiquitination. During acute oxidative stress, oxidized molecules modify the interaction of Nrf2 and Keap1, when Nrf2 is released from the cytoplasm into the nucleus where it binds to the antioxidant response element (ARE). This triggers the expression of antioxidant and detoxification genes. The consequence of long-term chronic oxidative stress is activation of glycogen synthase kinase 3β (GSK-3β) inhibiting Nrf2 activity and function. PPARγ (peroxisome proliferator-activated receptor gamma) is a nuclear receptor playing an important role in the management of cardiovascular diseases, hypertension and metabolic syndrome. PPARγ targeting of genes with peroxisome proliferator response element (PPRE) has led to the identification of several genes involved in lipid metabolism or oxidative stress. PPARγ stimulation is triggered by endogenous and exogenous ligands – agonists and it is involved in the activation of several cellular signaling pathways involved in oxidative stress response, such as the PI3K/Akt/NOS pathway. Nrf2 and PPARγ are linked together with their several activators and Nrf2/ARE and PPARγ/PPRE pathways can control several types of diseases.

A Comprehensive Review of Oxidative Stress as the Underlying Mechanism in Atherosclerosis and the Inefficiency of Antioxidants to Revert this Process

2019 ◽  
Vol 24 (40) ◽  
pp. 4705-4710 ◽  
Author(s):  
Kevin G. Cabezas ◽  
Carmen R. Gómez-Fernandez ◽  
Roberto Vazquez-Padron
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Reactive Oxygen ◽  
Underlying Mechanism ◽  
Plaque Formation ◽  
Oxygen Species ◽  
Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitors ◽  
Coa Reductase

Background: Cardiovascular diseases account for the highest mortality rate in the United States. The major underlying mechanism driving the onset and maintenance of cardiovascular diseases is atherosclerosis. Atherosclerosis is a chronic disease affecting large and medium-size arteries; it proceeds through four main stages along different decades of life, beginning at birth. Atherosclerosis is a consequence of oxidative stress, where homeostasis between endogenous antioxidants and reactive oxygen species is disrupted. Failure of intrinsic antioxidants and prophylactic antioxidant supplements to prevent atherosclerosis formation is an ongoing area of research in the race to avert, manage and cure atherosclerosis. Methods: The purpose of this work was to elucidate the actions of reactive oxygen species and oxidative stress on the formation of atherosclerosis as well as the different stages of atherosclerosis and the different mechanisms to prevent it. Through an extensive review of scientific literature, this paper correlates cell damage caused by oxidative stress to atheromatous plaque formation, as well as an in-depth analysis of high-density lipoproteins and enzymatic and non-enzymatic antioxidant role on atherosclerosis prevention. The antioxidant mechanism is overwhelmed by atherosclerotic processes and fails to be the ideal treatment of atherosclerosis. There is no scientific data that correlates prophylactic and non-prophylactic antioxidant treatment to a decrease in mortality or comorbidities pertaining to atherosclerosis. This is thought to be due to lack of consensus of optimal therapeutic doses, lack of reliable markers indicating which patient is to benefit from therapy and the chemical complexity of antioxidants in vivo. Current treatments for atherosclerosis include HMG-CoA reductase inhibitors which directly target low-density lipoproteins to tackle atherosclerotic plaque formation. Conclusion: HMG-CoA reductase inhibitors are not enough for the treatment of atherosclerosis given the complexity of the disease which has immune, musculoskeletal, genetic and hematologic aspects besides the involvement of lipids and lipoproteins. Therefore, other pharmacologic targets such as the PCSK9 enzyme and NFK- β should be researched in depth as possible treatments for atherosclerosis.

scholarly journals Dose-Dependent Effects of Cold Atmospheric Argon Plasma on the Mesenchymal Stem and Osteosarcoma Cells In Vitro

2021 ◽  
Vol 22 (13) ◽  
pp. 6797
Author(s):  
Artem M. Ermakov ◽  
Olga N. Ermakova ◽  
Vera A. Afanasyeva ◽  
Anton L. Popov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Stem Cells ◽  
Cancer Cells ◽  
Transcriptional Activity ◽  
Argon Plasma ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Normal Cells

The antimicrobial, anti-inflammatory and tissue-stimulating effects of cold argon atmospheric plasma (CAAP) accelerate its use in various fields of medicine. Here, we investigated the effects of CAAP at different radiation doses on mesenchymal stem cells (MSCs) and human osteosarcoma (MNNG/HOS) cells. We observed an increase in the growth rate of MSCs at sufficiently low irradiation doses (10–15 min) of CAAP, while the growth of MNNG/HOS cells was slowed down to 41% at the same irradiation doses. Using flow cytometry, we found that these effects are associated with cell cycle arrest and extended death of cancer cells by necrosis. Reactive oxygen species (ROS) formation was detected in both types of cells after 15 min of CAAP treatment. Evaluation of the genes’ transcriptional activity showed that exposure to low doses of CAAP activates the expression of genes responsible for proliferation, DNA replication, and transition between phases of the cell cycle in MSCs. There was a decrease in the transcriptional activity of most of the studied genes in MNNG/HOS osteosarcoma cancer cells. However, increased transcription of osteogenic differentiation genes was observed in normal and cancer cells. The selective effects of low and high doses of CAAP treatment on cancer and normal cells that we found can be considered in terms of hormesis. The low dose of cold argon plasma irradiation stimulated the vital processes in stem cells due to the slight generation of reactive oxygen species. In cancer cells, the same doses evidently lead to the formation of oxidative stress, which was accompanied by a proliferation inhibition and cell death. The differences in the cancer and normal cells’ responses are probably due to different sensitivity to exogenous oxidative stress. Such a selective effect of CAAP action can be used in the combined therapy of oncological diseases such as skin neoplasms, or for the removal of remaining cancer cells after surgical removal of a tumor.

Effect of The Autophagy Mechanism of TSCs Induced by Oxidative Stress Under Beclin1-mTOR Interaction

2021 ◽  
Author(s):  
Zhijun Liu ◽  
Shaojin Liu ◽  
Weipeng Zheng ◽  
Zhihao Liao ◽  
Sheng Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Rotator Cuff ◽  
Protein Expression ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Expression Levels ◽  
Rotator Cuff Injury

Abstract Background Tendinopathy is a chronic injury disease caused by repeated traction. It is characterized by exercise-related pain, increased local tendon sensitivity, and imaging changes in the tendon. Rotator cuff injury is one of the typical tendinopathy. Tendon-derived stem cells (TDSC) play a vital role in the development of tendinopathy. Our previous studies have found that reactive oxygen species increase after rotator cuff injury and the oxidative stress response is strengthened, but whether oxidative stress induces TDSC autophagy to promote tendon bone healing is not clear. Methods First, we collected the injured and normal tendon tissues of patients with rotator cuff injury, detected the levels of reactive oxygen species (ROS) and superoxide anion (SOD) in the tissues, detected Beclin1, mTOR gene expression by qPCR, and WB (Western blotting). Beclin1, p-mTOR/mTOR protein expression.Then, we extracted human tendon stem cells (TDSC) from tendon tissue, infected TDSC with recombinant lentivirus pLKO.1-shBeclin1, and verified the expression of Beclin1 by qPCR and WB.Finally, H2O2 and 3-MA were used to intervene TSCs. CCK8 was used to detect the proliferation ability of H2O2 on human TSCs; autophagy staining (MDC), autophagy-lysosome staining (Lyso-Tracker Red) and transmission electron microscopy were used to observe autophagy. Immunofluorescence staining detects the expression of autophagy factor LC3A/B; DCFH-DA detects cellular reactive oxygen species ROS level, Annexin V/PI detects cell apoptosis; WB detects Beclin1, mTOR, p-mTOR (Ser2448), LC3A/B, cleaved caspase-3 protein expression. Results In this study, it was found that the expression levels of ROS and Beclin1 in the damaged rotator cuff tissue were higher, while the expression levels of SOD and mTOR were lower. After the recombinant lentivirus pLKO.1-shBeclin1 was infected with TDSC, the expression of Beclin1 decreased. After treating TDSCs with H2O2 and 3-MA, it was found that H2O2 caused an increase in reactive oxygen species ROS content, autophagy levels, and LC3A/B expression in TDSCs, and an increase in Beclin1, mTOR, LC3A/B, and cleaved caspase-3 protein expression. Lead to a decrease in the level of apoptosis. Conclusion Under the mutual regulation of Beclin1-mTOR, oxidative stress induces the occurrence of autophagy in TSCs, and autophagy may protect TSCs from oxidative stress by reducing the accumulation of ROS.

Are reactive oxygen species important mediators of vascular dysfunction?

2019 ◽  
Vol 15 ◽  
Author(s):  
Gabriel T. do Vale ◽  
Carlos R. Tirapelli
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Vascular Dysfunction ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Ros Generation ◽  
Oxygen Species ◽  
Promising Alternative

Reactive oxygen species (ROS) are reactive derivatives of oxygen metabolism. The ROS generation can be mediated by distinctive enzymatic systems including NADPH oxidases. The components of this enzyme are expressed in endothelial and vascular smooth muscle cells, adventitial fibroblasts, and infiltrating monocytes/macrophages. Oxidative stress is a molecular dysregulation in ROS generation/elimination, which plays a key role in the development of vascular dysfunction in distinctive conditions including hypertension. It is characterized by vascular inflammation, a loss of NO bioavailability and endothelial dysfunction. Considering that oxidative stress is a key mediator of vascular dysfunction, antioxidant therapy with classic antioxidants seemed to be a promising alternative for the treatment of vascular diseases. In this sense, some commonly used drugs for the treatment of cardiovascular diseases such as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor AT1 antagonists showed antioxidant effects that might have contributed, at least in part, to the beneficial effects of these drugs on the treatment of cardiovascular diseases. The effectiveness of these drugs shows that ROS are in fact important mediators of vascular dysfunction and that angiotensin II plays a critical role in such response.

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