scholarly journals Characterization of TGF-β by Induced Oxidative Stress in Human Trabecular Meshwork Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 107
Author(s):  
Hsin-Yi Chen ◽  
Hsiu-Chuan Chou ◽  
Yi-Jung Ho ◽  
Shing-Jyh Chang ◽  
En-Chi Liao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
P38 Mapk ◽  
Trabecular Meshwork ◽  
Protein Level ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Trabecular Meshwork Cells ◽  
Tgf Β1

Oxidative stress generated by reactive oxygen species (ROS) plays a critical role in the pathomechanism of glaucoma, which is a multifactorial blinding disease that may cause irreversible damage within human trabecular meshwork cells (HTMCs). It is known that the transforming growth factor-β (TGF-β) signaling pathway is an important component of oxidative stress-induced damage related to extracellular matrix (ECM) fibrosis and activates cell antioxidative mechanisms. To elucidate the dual potential roles and regulatory mechanisms of TGF-β in effects on HTMCs, we established an in vitro oxidative model using hydrogen peroxide (H2O2) and further focused on TGF-β-related oxidative stress pathways and the related signal transduction. Via a series of cell functional qualitative analyses to detect related protein level alterations and cell fibrosis status, we illustrated the role of TGF-β1 and TGF-β2 in oxidative stress-induced injury by shTGF-β1 and shTGF-β2 knockdown or added recombinant human TGF-β1 protein (rhTGF-β1). The results of protein level showed that p38 MAPK, TGF-β, and its related SMAD family were activated after H2O2 stimulation. Cell functional assays showed that HTMCs with H2O2 exposure duration had a more irregular actin architecture compared to normal TM cells. Data with rhTGF-β1 (1 ng/mL) pretreatment reduced the cell apoptosis rate and amount of reactive oxygen species (ROS), while it also enhanced survival. Furthermore, TGF-β1 and TGF-β2 in terms of antioxidant signaling were related to the activation of collagen I and laminin, which are fibrosis-response proteins. Succinctly, our study demonstrated that low concentrations of TGF-β1 (1 ng/mL) preserves HTMCs from free radical-mediated injury by p-p38 MAPK level and p-AKT signaling balance, presenting a signaling transduction mechanism of TGF-β1 in HTMC oxidative stress-related therapies.

scholarly journals POSSIBLE PREVENTION OF REACTIVE OXYGEN SPECIES INDUCED HUMAN TRABECULAR MESHWORK CELL DAMAGE BY RESVERATROL AND ASCORBIC ACID.

2019 ◽  
Vol 26 (07) ◽  
pp. 1036-1041
Author(s):  
Muhammad Yaqoob Shahani ◽  
Umbreen Bano ◽  
Shazia Begum Shahani ◽  
Pashmina Shaikh ◽  
Sameena Gul Memon ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ascorbic Acid ◽  
Cell Viability ◽  
Trabecular Meshwork ◽  
Cell Metabolism ◽  
Cell Activity ◽  
Reactive Oxygen ◽  
Research Centre ◽  
Oxygen Species ◽  
Trabecular Meshwork Cells

Objectives: To analyze the antioxidant activity of Resveratrol and Ascorbic Acid against hydrogen peroxide (an oxidant) mediated cell injury of human trabecular meshwork cells. Study Design: Experimental study. Setting: Molecular Biology Laboratory at Medical Research Centre, Liaquat University of Medical & Health Sciences, Jamshoro. Period: Six months. Materials and Methods: Human Trabecular Meshwork cells were purchased from ScienCell Research Laboratories, USA. TM cell metabolism, TM cell viability and Reactive oxygen species were detected by standard methods in co- and pre- treated TM cells. Results: A significant reduction in TM cell metabolism was observed approximating 61% at 1.0 mM H2O2 compared to Ascorbate – 99% and Resveratrol 99% (p=0.0001). Resveratrol was more effective than Ascorbate even at 4.0 mM H2O2, the TM cell activity was noted 76%. Compared to H2O2- treated TM cells, resveratrol improved mitochondrial function upto 4.0 mM H2O2 (76%). Compared to co-treatment, the pretreatment shows similar results except at 4.0 mM H2O2. At 4.0 mM H2O2 the pre-treat TM cell metabolic activity was found as 11%, 31% and 47% compared to co-treat as 9%, 31% and 76% in controls, ascorbate and resveratrol groups respectively (p<0.05). Resveratrol shows significant decrease in viability was seen in controls compared to Ascorbate and Resveratrol groups. Cell viability showed statistically significant differences at 2.0 and 4.0 mM H2O2 compared to controls (P=0.0001). For reactive oxygen species (ROS), cells were incubated and with Ascorbate and Resveratrol for 24 hours and TM cells were treated with 0.0mM, 0.5 mM, 1.0 mM, 2.0mM and 4.0mM H2O2. Significant decrease in ROS was noted by Resveratrol compared to Ascorbate. Conclusions: Resveratrol and Ascorbate may prove useful in preventing and delaying the glaucoma, and timely institution of these anti – oxidants may help maintain trabecular meshwork functions and prevent visual loss.

scholarly journals High Potency of a Novel Resveratrol Derivative, 3,3′,4,4′-Tetrahydroxy-trans-stilbene, against Ovarian Cancer Is Associated with an Oxidative Stress-Mediated Imbalance between DNA Damage Accumulation and Repair

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Justyna Mikuła-Pietrasik ◽  
Patrycja Sosińska ◽  
Marek Murias ◽  
Marcin Wierzchowski ◽  
Marta Brewińska-Olchowik ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Ovarian Cancer ◽  
Dna Damage ◽  
P38 Mapk ◽  
Cancer Cell ◽  
Damage Accumulation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Stress Dependent

We explored the effect of a new resveratrol (RVT) derivative, 3,3′,4,4′-tetrahydroxy-trans-stilbene (3,3′,4,4′-THS), on viability, apoptosis, proliferation, and senescence of three representative lines of ovarian cancer cells, that is, A2780, OVCAR-3, and SKOV-3,in vitro. In addition, the mechanistic aspects of 3,3′,4,4′-THS activity, including cell redox homeostasis (the production of reactive oxygen species, activity of enzymatic antioxidants, and magnitude of DNA damage accumulation and repair), and the activity of caspases (3, 8, and 9) and p38 MAPK were examined. The study showed that 3,3′,4,4′-THS affects cancer cell viability much more efficiently than its parent drug. This effect coincided with increased generation of reactive oxygen species, downregulated activity of superoxide dismutase and catalase, and excessive accumulation of 8-hydroxy-2′-deoxyguanosine and its insufficient repair due to decreased expression of DNA glycosylase I. Cytotoxicity elicited by 3,3′,4,4′-THS was related to increased incidence of apoptosis, which was mediated by caspases 3 and 9. Moreover, 3,3′,4,4′-THS inhibited cancer cell proliferation and accelerated senescence, which was accompanied by the activation of p38 MAPK. Collectively, our findings indicate that 3,3′,4,4′-THS may constitute a valuable tool in the fight against ovarian malignancy and that the anticancer capabilities of this stilbene proceed in an oxidative stress-dependent mechanism.

scholarly journals Cigarette Smoke Promotes Interleukin-8 Production in Alveolar Macrophages Through the Reactive Oxygen Species/Stromal Interaction Molecule 1/Ca2+ Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Xianying Zhu ◽  
Yuan Zhan ◽  
Yiya Gu ◽  
Qian Huang ◽  
Ting Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Stromal Interaction Molecule 1 ◽  
Copd Patients

Chronic obstructive pulmonary disease (COPD), primarily attributed to cigarette smoke (CS), is characterized by multiple pathophysiological changes, including oxidative stress and inflammation. Stromal interaction molecule 1 (STIM1) is a Ca2+ sensor that regulates Ca2+ entry in different types of cells. The present study aimed to explore the relationship between CS-induced oxidative stress and inflammation, as well as the functional role of STIM1 thereinto. Our results showed that the reactive oxygen species (ROS)/STIM1/Ca2+ axis played a critical role in CS-induced secretion of interleukin (IL)-8 in human alveolar macrophages. Specifically, smokers with COPD (SC) showed higher levels of ROS in the lung tissues compared with healthy non-smokers (HN). STIM1 was upregulated in the lung tissues of COPD patients. The expression of STIM1 was positively associated with ROS levels and negatively correlated with pulmonary function. The expression of STIM1 was also increased in the bronchoalveolar lavage fluid (BALF) macrophages of COPD patients and PMA-differentiated THP-1 macrophages stimulated by cigarette smoke extract (CSE). Additionally, CSE-induced upregulation of STIM1 in PMA-differentiated THP-1 macrophages was inhibited by pretreatment with N-acetylcysteine (NAC), a ROS scavenger. Transfection with small interfering RNA (siRNA) targeting STIM1 and pretreatment with NAC alleviated CSE-induced increase in intracellular Ca2+ levels and IL-8 expression. Furthermore, pretreatment with SKF-96365 and 2-APB, the inhibitors of Ca2+ influx, suppressed CSE-induced secretion of IL-8. In conclusion, our study demonstrates that CSE-induced ROS production may increase the expression of STIM1 in macrophages, which further promotes the release of IL-8 by regulating Ca2+ entry. These data suggest that STIM1 may play a crucial role in CSE-induced ROS production and inflammation, and participate in the pathogenesis of COPD.

scholarly journals Reactive Oxygen Species in Neurodegenerative Diseases: Implications in Pathogenesis and Treatment Strategies

2021 ◽  
Author(s):  
Johnson Olaleye Oladele ◽  
Adenike T. Oladiji ◽  
Oluwaseun Titilope Oladele ◽  
Oyedotun M. Oyeleke
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Protein Misfolding ◽  
Critical Role ◽  
Treatment Strategies ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
The Brain

Neurodegenerative diseases are debilitating disorders which compromise motor or cognitive functions and are rapidly becoming a global communal disorder with over 46.8 million people suffering dementia worldwide. Aetiological studies have showed that people who are exposed to agricultural, occupational and environmental toxic chemicals that can interfere and degenerate dopaminergic neurons are prone to developing neurodegenerative diseases such as Parkinson Disease. The complex pathogenesis of the neurodegenerative diseases remains largely unknown; however, mounting evidence suggests that oxidative stress, neuroinflammation, protein misfolding, and apoptosis are the hallmarks of the diseases. Reactive oxygen species (ROS) are chemically reactive molecules that have been implicated in the pathogenesis of neurodegenerative diseases. ROS play a critical role as high levels of oxidative stress are commonly observed in the brain of patients with neurodegenerative disorders. This chapter focus on the sources of ROS in the brain, its involvement in the pathogenesis of neurodegenerative diseases and possible ways to mitigate its damaging effects in the affected brain.

scholarly journals Reactive Oxygen Species (ROS), Oxidative Stress and its role In HIV Infection

2020 ◽  
Vol 11 (3) ◽  
pp. 4560-4568
Author(s):  
Sunita S Patil ◽  
Vaishali S Patil ◽  
Arvind Gulbake
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hiv Infection ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Hiv Patients ◽  
Signalling Molecules ◽  
The Impact

Throughout several regular cell cycles, reactive oxygen species (ROS) play a critical role. When ROS values are high, and when the defence mechanism (antioxidants) cannot neutralise, they harm and modify the part of biological molecules. They also act as signalling molecules which generate a spectrum of disease.In this study, we reviewed existing oxidants, oxidative stress, and their relationship with infection by human immunodeficiency virus in patients, and the effects of oxidative stress in patients with HIV.Our prospect is to do a clinical study on HIV patients and estimate oxidative parameters like nitric oxide, total antioxidant level and correlate them with CD4 count and viral load which may be helpful during monitoring and giving efficient ART to the HIV patients. And also the importance of ROS in infection has been established through clinical and in vitro studies. Here we review the role of oxidative stress in HIV pathogenesis, the impact of ROS on immune responses in HIV patients, and ROS-mediated regulation of HIV infection. Future studies on the interplay between ROS and HIV infection may offer a new strategy for prevention and treatment.

scholarly journals Cytoprotective Role of Omentin Against Oxidative Stress-Induced Vascular Endothelial Cells Injury

Molecules ◽  
2020 ◽  
Vol 25 (11) ◽  
pp. 2534 ◽  
Author(s):  
Nur Aqilah Binti Kamaruddin ◽  
Lai Yen Fong ◽  
Jun Jie Tan ◽  
Muhammad Nazrul Hakim Abdullah ◽  
Manraj Singh Cheema ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Mtt Assay ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Gpx Activity

Endothelial cell injury caused by reactive oxygen species (ROS) plays a critical role in the pathogenesis of cardiovascular diseases. Omentin, an adipocytokine that is abundantly expressed in visceral fat tissue, has been reported to possess anti-inflammatory and antidiabetic properties. However, endothelial protective effects of omentin against oxidative stress remain unclear. This study aimed to evaluate the protective effect of omentin against hydrogen peroxide (H2O2)-induced cell injury in human umbilical vein endothelial cells (HUVECs). Cytotoxicity and cytoprotective effects of omentin were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptotic activity of HUVECs was detected using Annexin-V/PI and Hoechst 33258 staining methods. Antioxidant activity of omentin was evaluated by measuring both reactive oxygen species (ROS) levels and glutathione peroxidase (GPx) activity. No cytotoxicity effect was observed in HUVECs treated with omentin alone at concentrations of 150 to 450 ng/ml. MTT assay showed that omentin significantly prevented the cell death induced by H2O2 (p < 0.001). Hoechst staining and flow cytometry also revealed that omentin markedly prevented H2O2-induced apoptosis. Moreover, omentin not only significantly inhibited ROS production (p < 0.01) but also significantly (p < 0.01) increased GPx activity in HUVECs. In conclusion, our data suggest that omentin may protect HUVECs from injury induced by H2O2.

Reactive oxygen species/oxidative stress contributes to progression of kidney fibrosis following transient ischemic injury in mice

2009 ◽  
Vol 297 (2) ◽  
pp. F461-F470 ◽  
Author(s):  
Jinu Kim ◽  
Young Mi Seok ◽  
Kyong-Jin Jung ◽  
Kwon Moo Park
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Smooth Muscle Actin ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Kidney Fibrosis ◽  
Copper Zinc ◽  
Glucose 6 Phosphate Dehydrogenase

Recently, kidney fibrosis following transplantation has become recognized as a main contributor of chronic allograft nephropathy. In transplantation, transient ischemia is an inescapable event. Reactive oxygen species (ROS) play a critical role in ischemia and reperfusion (I/R)-induced acute kidney injury, as well as progression of fibrosis in various diseases such as hypertension, diabetes, and ureteral obstruction. However, a role of ROS/oxidative stress in chronic kidney fibrosis following I/R injury remains to be defined. In this study, we investigated the involvement of ROS/oxidative stress in kidney fibrosis following kidney I/R in mice. Mice were subjected to 30 min of bilateral kidney ischemia followed by reperfusion on day 0 and then administered with either manganese (III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP, 5 mg/kg body wt ip), a cell permeable superoxide dismutase (SOD) mimetic, or 0.9% saline (vehicle) beginning at 48 h after I/R for 14 days. I/R significantly increased interstitial extension, collagen deposition, apoptosis of tubular epithelial cells, nitrotyrosine expression, hydrogen peroxide production, and lipid peroxidation and decreased copper-zinc SOD, manganese SOD, and glucose 6-phosphate dehydrogenase activities in the kidneys 16 days after the procedure. MnTMPyP administration minimized these postischemic changes. In addition, MnTMPyP administration significantly attenuated the increases of α-smooth muscle actin, PCNA, S100A4, CD68, and heat shock protein 47 expression following I/R. We concluded that kidney fibrosis develops chronically following I/R injury, and this process is associated with the increase of ROS/oxidative stress.

scholarly journals Antioxidants Maintain Cellular Redox Homeostasis by Elimination of Reactive Oxygen Species

2017 ◽  
Vol 44 (2) ◽  
pp. 532-553 ◽  
Author(s):  
Long He ◽  
Ting He ◽  
Shabnam Farrar ◽  
Linbao Ji ◽  
Tianyi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Signaling Molecules ◽  
Antioxidant Systems ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Cytochrome P450 Enzymes ◽  
Cell Death Pathway

Reactive oxygen species (ROS) are produced by living cells as normal cellular metabolic byproduct. Under excessive stress conditions, cells will produce numerous ROS, and the living organisms eventually evolve series of response mechanisms to adapt to the ROS exposure as well as utilize it as the signaling molecules. ROS molecules would trigger oxidative stress in a feedback mechanism involving many biological processes, such as apoptosis, necrosis and autophagy. Growing evidences have suggested that ROS play a critical role as the signaling molecules throughout the entire cell death pathway. Overwhelming production of ROS can destroy organelles structure and bio-molecules, which lead to inflammatory response that is a known underpinning mechanism for the development of diabetes and cancer. Cytochrome P450 enzymes (CYP) are regarded as the markers of oxidative stress, can transform toxic metabolites into ROS, such as superoxide anion, hydrogen peroxide and hydroxyl radical which might cause injury of cells. Accordingly, cells have evolved a balanced system to neutralize the extra ROS, namely antioxidant systems that consist of enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidases (GPxs), thioredoxin (Trx) as well as the non-enzymatic antioxidants which collectively reduce oxidative state. Herein, we review the recent novel findings of cellular processes induced by ROS, and summarize the roles of cellular endogenous antioxidant systems as well as natural anti-oxidative compounds in several human diseases caused by ROS in order to illustrate the vital role of antioxidants in prevention against oxidative stress.

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