scholarly journals SPARC Levels Modulate the Capacity of Mitomycin to Inhibit the Proliferation of Human Tenon’s Capsule Fibroblasts

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yuanyuan Guo ◽  
Shouxiang Ni ◽  
Weiyan Zhou ◽  
Jiangping Hou ◽  
Jiaquan Shen
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Density ◽  
Collagen Gel ◽  
Reactive Oxygen ◽  
Control Group ◽  
Mrna Levels ◽  
Oxygen Species ◽  
Antifibrotic Effect ◽  
Cell Densities

Purpose. To evaluate the role of SPARC in the antiproliferation effect of MMC on human Tenon’s fibroblasts (HTF). Method. Sixteen PACG patients aged 59 ± 10 years (31–72 years), including 6 males and 10 females, were recruited. Tenon tissue was harvested during filtering surgery. Cell density was evaluated after MMC application with different concentrations and application times, by which the optimized MMC application modality was determined. MMC, si-SPARC, or SPARC protein was used when needed to evaluate the cell densities under different conditions, by which the role of SPARC in MMC-mediated antifibrotic process was identified. Results. Considering that the cell densities, as well as SPARC expression on mRNA and protein levels, are relatively stable when the MMC concentration is higher than 0.02% and exposure time longer than 90 s, we chose the MMC application pattern with 0.02% and 90 s as an optimized pattern for the downstream work. Compared to control, the si-SPARC and MMC downregulated the SPARC protein by 91% (P<0.01) and 65% (P<0.01) and mRNA by 96% (P<0.01) and 64% (P<0.01), respectively. MMC decreases the cell densities by 53.50% compared to control. si-SPARC + MMC dramatically deceased the cell density no matter compared to the control group (P<0.01) or MMC group (P<0.01); correspondingly, the relative collagen gel area in the MMC + si-SPARC group was higher than that in the MMC group or si-SPARC group (P<0.05). The reactive oxygen species expression in the MMC + si-SPARC group is higher than that in the MMC group (P<0.05). Conclusion. This study demonstrates that in HTF, (1) MMC downregulates the expression of SPARC in protein and mRNA levels; (2) SPARC depletion has synergistic effect on the antifibrotic effect of MMC; and (3) reactive oxygen species are the possible mediator in the antifibrotic effect of MMC and si-SPARC.

Reactive oxygen species modulate HIF-1 mediated PAI-1 expression: involvement of the GTPase Rac1

2003 ◽  
Vol 89 (05) ◽  
pp. 926-935 ◽  
Author(s):  
Utta Berchner-Pfannschmidt ◽  
Christoph Wotzlaw ◽  
Robbert Cool ◽  
Joachim Fandrey ◽  
Helmut Acker ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Plasminogen Activator Inhibitor ◽  
Dominant Negative ◽  
Mrna Levels ◽  
Ros Production ◽  
Oxygen Species ◽  
Plasminogen Activator Inhibitor 1 ◽  
Pai 1

SummaryThe hypoxia-inducible transcription factor HIF-1 mediates upregulation of plasminogen activator inhibitor-1 (PAI-1) expression under hypoxia. Reactive oxygen species (ROS) have also been implicated in PAI-1 gene expression. However, the role of ROS in HIF-1-mediated regulation of PAI-1 is not clear. We therefore investigated the role of the GTPase Rac1 which modulates ROS production in the pathway leading to HIF-1 and PAI-1 induction.Overexpression of constitutively activated (RacG12V) or dominant-negative (RacT17N) Rac1 increased or decreased, respectively, ROS production. In RacG12V-expressing cells, PAI-1 mRNA levels as well as HIF-1α nuclear presence were reduced under normoxia and hypoxia whereas expression of RacT17N resulted in opposite effects. Treatment with the antioxidant pyrrolidinedithiocarbamate or coexpression of the redox factor-1 restored HIF-1 and PAI-1 promoter activity in RacG12V-cells. In contrast, NFκB activation was enhanced in RacG12V-cells, but abolished by RacT17N. Thus, these findings suggest a mechanism explaining modified fibrinolysis and tissue remodeling in an oxidized environment.

scholarly journals Myeloperoxidase activity in blood plasma as a criterion of therapy for patients with cardiovascular disease

2016 ◽  
Vol 62 (3) ◽  
pp. 318-324 ◽  
Author(s):  
D.V. Grigorieva ◽  
I.V. Gorudko ◽  
V.A. Kostevich ◽  
A.V. Sokolov ◽  
I.V. Buko ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Plasma Concentrations ◽  
Reactive Oxygen ◽  
Molar Ratio ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Oxygen Species ◽  
Coronary Syndrome ◽  
Neutrophil Degranulation

A significant increase in the myeloperoxidase (MPO) activity has been found in plasma of patients with stable angina and with acute coronary syndrome (ACS) in comparison with the control group. MPO concentration was significantly increased in plasma of ACS patients. Reduced MPO activity in the treated ACS patients correlated with a favorable outcome of the disease. Generally, changes in plasma MPO concentration coincided with changes in lactoferrin concentration thus confirming the role of neutrophil degranulation in the increase of plasma concentrations of these proteins. The increase in MPO activity was obviously determined by modification of the MPO protein caused by reactive oxygen species and halogen in the molar ratio of 1 : 25 and 1 : 50. The decrease in plasma MPO activity may be associated with increased plasma concentrations of the physiological inhibitor of its activity, ceruloplasmin, and also with modification of the MPO protein with reactive oxygen species and halogen at their molar ratio of 1 : 100 and higher. Thus, MPO activity may be used for evaluation of effectiveness of the treatment of cardiovascular diseases.

scholarly journals Identification of Pathways and Key Genes in Carotid Atherosclerosis by Bioinformatics Analysis

2021 ◽  
Author(s):  
Di Zhang ◽  
Bei Jing ◽  
Xin Li ◽  
Huimei Shi ◽  
Shiquan Chang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Palmitic Acid ◽  
Experimental Verification ◽  
Carotid Atherosclerosis ◽  
Mrna Level ◽  
Reactive Oxygen ◽  
Control Group ◽  
Mrna Levels ◽  
Oxygen Species ◽  
Huvec Cells

Abstract Purpose: Carotid atherosclerosis is a serious vascular disease, leading to various cerebrovascular diseases. Methods: Gene expression profile of GSE100927 was selected to conduct differentially expressed genes. Then we performed protein-protein interactions, Gene ontology, and Kyoto Encyclopedia of Genes and Genomes analysis. Then we used HUVEC, HAVSMC, and THP-1 induced macrophages cells to conduct experimental verification. The experimental groups were as follows: Control group, Solvent control group, and Palmitic acid group. We measured the levels of reactive oxygen species in three cells via flow cytometer or fluorescence microscope. Then we detected apoptosis of HUVEC cells and HAVSMC cells or observed nucleus of THP-1 induced macrophages cells. Results: We selected male carotid atherosclerosis, with 10 control samples and 21 atherosclerosis samples. The results of pathway enrichment showed that “Toll-like receptor signaling pathway” ranked first. We chose IL1β, CCL4, SPP1, CCL3, IRF5. MMP7 and MMP9 for experimental verification. Palmitic acid increased the reactive oxygen species levels and the apoptosis rates of HUVEC cells and HAVSMC cells while increasing the activity of THP-1 induced macrophages cells, and it cannot increase the level of reactive oxygen species, and shrink the nucleus. Palmitic acid increased mRNA levels of IL1β, CCL4, SPP1, CCL3, IRF5. MMP7 and MMP9 in HUVEC cells and THP-1 induced macrophages, and increased the mRNA levels of CCL4 and MMP9 in HAVSMC cells，not changed the mRNA level of IRF5. Conclusion: IL1β，CCL3, CCL4, SPP1, IRF5, MMP7, and MMP9 are significant markers of carotid atherosclerosis.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

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