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Kannadasan Anandbabu - One of the best experts on this subject based on the ideXlab platform.
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oxidized ldl homocysteine homocysteine thiolactone and advanced glycation end products act as pro oxidant metabolites inducing cytokine release macrophage infiltration and pro angiogenic effect in arpe 19 cells
PLOS ONE, 2019Co-Authors: Kannadasan Anandbabu, Narayanasamy AngayarkanniAbstract:Age-related Macular Degeneration (AMD) is one of the major vision-threatening diseases of the eye. Oxidative stress is one of the key factors in the onset and progression of AMD. In this study, metabolites associated with AMD pathology more so at the systemic level namely, oxidized LDL (oxLDL), homocysteine (Hcy), homocysteine thiolactone (HCTL), advanced glycation end product (AGE) were evaluated for their Pro-Oxidant nature in a localized ocular environment based on in vitro studies in human retinal pigment epithelial cells (ARPE-19 cells). Human ARPE-19 cells were treated with Pro-Oxidants 50 μg/mL oxLDL, 500 μM Hcy, 500 nM HCTL, 100 μg/mL AGE, 200 μM H2O2 and 200 μM H2O2 with and without pre-treatment of 5 mM N-acetyl cysteine (NAC). The cytokines IL-6, IL-8 and vascular endothelial growth factor (VEGF) secreted from ARPE-19 cells exposed to Pro-Oxidants were estimated by ELISA. In vitro angiogenesis assay was performed with conditioned media of the Pro-Oxidant treated ARPE-19 cells in Geltrex-Matrigel coated 96-well plate. The human acute monocytic leukemia cell line (THP-1) was differentiated into macrophages and its migration in response to conditioned media of ARPE-19 cells insulted with the Pro-Oxidants was studied by transwell migration assay. Western blot was performed to detect the protein expression of Bax, Bcl-2 and NF-κB to assess apoptotic changes. The compounds involved in the study showed a significant increase in reactive oxygen species (ROS) generation in ARPE-19 cells (oxLDL; Hcy; AGE: p < 0.001 and HCTL: p < 0.05). NAC pre-treatment significantly lowered the oxidative stress brought about by Pro-Oxidants as seen by lowered ROS and MDA levels in the cells. Treatment with Pro-Oxidants significantly increased the secretion of IL-6 (oxLDL: p < 0.05; Hcy, HCTL and AGE: p < 0.01) and IL-8 cytokines (oxLDL: p < 0.05; HCTL: p <. 001 and AGE: p < 0.01) in ARPE-19 cells. Serum samples of AMD patients (n = 23) revealed significantly higher IL-6 and IL-8 levels compared to control subjects (n = 23) (IL6: p < 0.01 and IL8: p < 0.05). The Pro-Oxidants also promoted VEGF secretion by ARPE-19 cells compared to untreated control (oxLDL: p < 0.001; Hcy: p < 0.01; HCTL and AGE: p < 0.05). In vitro angiogenesis assay showed that the conditioned media significantly increased the tube formation in RF/6A endothelial cells. Transwell migration assay revealed significant infiltration of macrophages in response to Pro-Oxidants. We further demonstrated that the Pro-Oxidants increased the Bax/Bcl-2 ratio and increased the NF-κB activation resulting in pro-apoptotic changes in ARPE-19 cells. Thus, oxLDL, Hcy, HCTL and AGE act as Pro-Oxidant metabolites in RPE that promote AMD through oxidative stress, inflammation, chemotaxis and neovascularization.
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Oxidized LDL, homocysteine, homocysteine thiolactone and advanced glycation end products act as Pro-Oxidant metabolites inducing cytokine release, macrophage infiltration and pro-angiogenic effect in ARPE-19 cells
2019Co-Authors: Kannadasan Anandbabu, Parveen Sen, Narayanasamy AngayarkanniAbstract:Age-related Macular Degeneration (AMD) is one of the major vision-threatening diseases of the eye. Oxidative stress is one of the key factors in the onset and progression of AMD. In this study, metabolites associated with AMD pathology more so at the systemic level namely, oxidized LDL (oxLDL), homocysteine (Hcy), homocysteine thiolactone (HCTL), advanced glycation end product (AGE) were evaluated for their Pro-Oxidant nature in a localized ocular environment based on in vitro studies in human retinal pigment epithelial cells (ARPE-19 cells). Human ARPE-19 cells were treated with Pro-Oxidants 50 μg/mL oxLDL, 500 μM Hcy, 500 nM HCTL, 100 μg/mL AGE, 200 μM H2O2 and 200 μM H2O2 with and without pre-treatment of 5 mM N-acetyl cysteine (NAC). The cytokines IL-6, IL-8 and vascular endothelial growth factor (VEGF) secreted from ARPE-19 cells exposed to Pro-Oxidants were estimated by ELISA. In vitro angiogenesis assay was performed with conditioned media of the Pro-Oxidant treated ARPE-19 cells in Geltrex-Matrigel coated 96-well plate. The human acute monocytic leukemia cell line (THP-1) was differentiated into macrophages and its migration in response to conditioned media of ARPE-19 cells insulted with the Pro-Oxidants was studied by transwell migration assay. Western blot was performed to detect the protein expression of Bax, Bcl-2 and NF-κB to assess apoptotic changes. The compounds involved in the study showed a significant increase in reactive oxygen species (ROS) generation in ARPE-19 cells (oxLDL; Hcy; AGE: p < 0.001 and HCTL: p < 0.05). NAC pre-treatment significantly lowered the oxidative stress brought about by Pro-Oxidants as seen by lowered ROS and MDA levels in the cells. Treatment with Pro-Oxidants significantly increased the secretion of IL-6 (oxLDL: p < 0.05; Hcy, HCTL and AGE: p < 0.01) and IL-8 cytokines (oxLDL: p < 0.05; HCTL: p
Narayanasamy Angayarkanni - One of the best experts on this subject based on the ideXlab platform.
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oxidized ldl homocysteine homocysteine thiolactone and advanced glycation end products act as pro oxidant metabolites inducing cytokine release macrophage infiltration and pro angiogenic effect in arpe 19 cells
PLOS ONE, 2019Co-Authors: Kannadasan Anandbabu, Narayanasamy AngayarkanniAbstract:Age-related Macular Degeneration (AMD) is one of the major vision-threatening diseases of the eye. Oxidative stress is one of the key factors in the onset and progression of AMD. In this study, metabolites associated with AMD pathology more so at the systemic level namely, oxidized LDL (oxLDL), homocysteine (Hcy), homocysteine thiolactone (HCTL), advanced glycation end product (AGE) were evaluated for their Pro-Oxidant nature in a localized ocular environment based on in vitro studies in human retinal pigment epithelial cells (ARPE-19 cells). Human ARPE-19 cells were treated with Pro-Oxidants 50 μg/mL oxLDL, 500 μM Hcy, 500 nM HCTL, 100 μg/mL AGE, 200 μM H2O2 and 200 μM H2O2 with and without pre-treatment of 5 mM N-acetyl cysteine (NAC). The cytokines IL-6, IL-8 and vascular endothelial growth factor (VEGF) secreted from ARPE-19 cells exposed to Pro-Oxidants were estimated by ELISA. In vitro angiogenesis assay was performed with conditioned media of the Pro-Oxidant treated ARPE-19 cells in Geltrex-Matrigel coated 96-well plate. The human acute monocytic leukemia cell line (THP-1) was differentiated into macrophages and its migration in response to conditioned media of ARPE-19 cells insulted with the Pro-Oxidants was studied by transwell migration assay. Western blot was performed to detect the protein expression of Bax, Bcl-2 and NF-κB to assess apoptotic changes. The compounds involved in the study showed a significant increase in reactive oxygen species (ROS) generation in ARPE-19 cells (oxLDL; Hcy; AGE: p < 0.001 and HCTL: p < 0.05). NAC pre-treatment significantly lowered the oxidative stress brought about by Pro-Oxidants as seen by lowered ROS and MDA levels in the cells. Treatment with Pro-Oxidants significantly increased the secretion of IL-6 (oxLDL: p < 0.05; Hcy, HCTL and AGE: p < 0.01) and IL-8 cytokines (oxLDL: p < 0.05; HCTL: p <. 001 and AGE: p < 0.01) in ARPE-19 cells. Serum samples of AMD patients (n = 23) revealed significantly higher IL-6 and IL-8 levels compared to control subjects (n = 23) (IL6: p < 0.01 and IL8: p < 0.05). The Pro-Oxidants also promoted VEGF secretion by ARPE-19 cells compared to untreated control (oxLDL: p < 0.001; Hcy: p < 0.01; HCTL and AGE: p < 0.05). In vitro angiogenesis assay showed that the conditioned media significantly increased the tube formation in RF/6A endothelial cells. Transwell migration assay revealed significant infiltration of macrophages in response to Pro-Oxidants. We further demonstrated that the Pro-Oxidants increased the Bax/Bcl-2 ratio and increased the NF-κB activation resulting in pro-apoptotic changes in ARPE-19 cells. Thus, oxLDL, Hcy, HCTL and AGE act as Pro-Oxidant metabolites in RPE that promote AMD through oxidative stress, inflammation, chemotaxis and neovascularization.
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Oxidized LDL, homocysteine, homocysteine thiolactone and advanced glycation end products act as Pro-Oxidant metabolites inducing cytokine release, macrophage infiltration and pro-angiogenic effect in ARPE-19 cells
2019Co-Authors: Kannadasan Anandbabu, Parveen Sen, Narayanasamy AngayarkanniAbstract:Age-related Macular Degeneration (AMD) is one of the major vision-threatening diseases of the eye. Oxidative stress is one of the key factors in the onset and progression of AMD. In this study, metabolites associated with AMD pathology more so at the systemic level namely, oxidized LDL (oxLDL), homocysteine (Hcy), homocysteine thiolactone (HCTL), advanced glycation end product (AGE) were evaluated for their Pro-Oxidant nature in a localized ocular environment based on in vitro studies in human retinal pigment epithelial cells (ARPE-19 cells). Human ARPE-19 cells were treated with Pro-Oxidants 50 μg/mL oxLDL, 500 μM Hcy, 500 nM HCTL, 100 μg/mL AGE, 200 μM H2O2 and 200 μM H2O2 with and without pre-treatment of 5 mM N-acetyl cysteine (NAC). The cytokines IL-6, IL-8 and vascular endothelial growth factor (VEGF) secreted from ARPE-19 cells exposed to Pro-Oxidants were estimated by ELISA. In vitro angiogenesis assay was performed with conditioned media of the Pro-Oxidant treated ARPE-19 cells in Geltrex-Matrigel coated 96-well plate. The human acute monocytic leukemia cell line (THP-1) was differentiated into macrophages and its migration in response to conditioned media of ARPE-19 cells insulted with the Pro-Oxidants was studied by transwell migration assay. Western blot was performed to detect the protein expression of Bax, Bcl-2 and NF-κB to assess apoptotic changes. The compounds involved in the study showed a significant increase in reactive oxygen species (ROS) generation in ARPE-19 cells (oxLDL; Hcy; AGE: p < 0.001 and HCTL: p < 0.05). NAC pre-treatment significantly lowered the oxidative stress brought about by Pro-Oxidants as seen by lowered ROS and MDA levels in the cells. Treatment with Pro-Oxidants significantly increased the secretion of IL-6 (oxLDL: p < 0.05; Hcy, HCTL and AGE: p < 0.01) and IL-8 cytokines (oxLDL: p < 0.05; HCTL: p
Pak H Chan - One of the best experts on this subject based on the ideXlab platform.
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oxidative stress in ischemic brain damage mechanisms of cell death and potential molecular targets for neuroprotection
Antioxidants & Redox Signaling, 2011Co-Authors: Hai Chen, Hideyuki Yoshioka, Joo Eun Jung, Nobuya Okami, Hiroyuki Sakata, Carolina M Maier, Purnima Narasimhan, Christina E Goeders, Pak H ChanAbstract:Abstract Significant amounts of oxygen free radicals (oxidants) are generated during cerebral ischemia/reperfusion, and oxidative stress plays an important role in brain damage after stroke. In addition to oxidizing macromolecules, leading to cell injury, oxidants are also involved in cell death/survival signal pathways and cause mitochondrial dysfunction. Experimental data from laboratory animals that either overexpress (transgenic) or are deficient in (knock-out) antioxidant proteins, mainly superoxide dismutase, have provided strong evidence of the role of oxidative stress in ischemic brain damage. In addition to mitochondria, recent reports demonstrate that NADPH oxidase (NOX), an important Pro-Oxidant enzyme, is also involved in the generation of oxidants in the brain after stroke. Inhibition of NOX is neuroprotective against cerebral ischemia. We propose that superoxide dismutase and NOX activity in the brain is a major determinant for ischemic damage/repair and that these major anti- and pro-oxidan...
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oxidative stress in ischemic brain damage mechanisms of cell death and potential molecular targets for neuroprotection
Antioxidants & Redox Signaling, 2011Co-Authors: Hai Chen, Hideyuki Yoshioka, Joo Eun Jung, Nobuya Okami, Hiroyuki Sakata, Carolina M Maier, Purnima Narasimhan, Christina E Goeders, Gab Seok Kim, Pak H ChanAbstract:Abstract Significant amounts of oxygen free radicals (oxidants) are generated during cerebral ischemia/reperfusion, and oxidative stress plays an important role in brain damage after stroke. In addition to oxidizing macromolecules, leading to cell injury, oxidants are also involved in cell death/survival signal pathways and cause mitochondrial dysfunction. Experimental data from laboratory animals that either overexpress (transgenic) or are deficient in (knock-out) antioxidant proteins, mainly superoxide dismutase, have provided strong evidence of the role of oxidative stress in ischemic brain damage. In addition to mitochondria, recent reports demonstrate that NADPH oxidase (NOX), an important Pro-Oxidant enzyme, is also involved in the generation of oxidants in the brain after stroke. Inhibition of NOX is neuroprotective against cerebral ischemia. We propose that superoxide dismutase and NOX activity in the brain is a major determinant for ischemic damage/repair and that these major anti- and pro-oxidan...
Emo Chiellini - One of the best experts on this subject based on the ideXlab platform.
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oxidation and biodegradation of polyethylene films containing pro oxidant additives synergistic effects of sunlight exposure thermal aging and fungal biodegradation
Polymer Degradation and Stability, 2010Co-Authors: Andrea Corti, Sudhakar Muniyasamy, Manuele Vitali, Syed H Imam, Emo ChielliniAbstract:Abstract Synergistic effects of sunlight exposure, thermal aging and fungal biodegradation on the oxidation and biodegradation of linear low density poly(ethylene) PE-LLD films containing Pro-Oxidant were examined. To achieve oxidation and degradation, films were first exposed to the sunlight for 93 days during the summer months followed by their incubation with fungal strains previously isolated from the soil based on the ability to grow on the oxidized PE-LLD as a sole carbon source. Some films were also thermally aged at temperatures ranging between 45°C and 65 °C, either before or after fungal degradation. Films with Pro-Oxidant additives exhibited a higher level of oxidation as revealed by increase in their carbonyl index (CO i ). In addition to increase in the CO i , films showed a slight increase in crystallinity and melting temperature ( T m ), considerably lower onset degradation temperatures, and a concomitant increase in the % weight of the residues. The level of oxidation observed in thermally aged films was directly proportional to the aging temperature. The PE-LLD films with Pro-Oxidant exposed to sunlight followed by thermal aging showed even higher rate and extent of oxidation when subsequently subjected to fungal biodegradation. The higher oxidation rate also correlated well with the CO 2 production in the fungal biodegradation tests. Similar films oxidized and aged but not exposed to fungal biodegradation showed much less degradation. Microscopic examination showed a profuse growth and colonization of fungal mycelia on the oxidized films by one strain, while another spore-producing strain grew around the film edges. Data presented here suggest that abiotic oxidation of polymer's carbon backbone produced metabolites which supported metabolic activities in fungal cells leading to further biotically-mediated polymer degradation. Thus, a combined impact of abiotic and biotic factors promoted the oxidation/biodegradation of PE-LLD films containing Pro-Oxidants.
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oxidation and biodegradation of polyethylene films containing pro oxidant additives synergistic effects of sunlight exposure thermal aging and fungal biodegradation
Polymer Degradation and Stability, 2010Co-Authors: Andrea Corti, Sudhakar Muniyasamy, Manuele Vitali, Syed H Imam, Emo ChielliniAbstract:Abstract Synergistic effects of sunlight exposure, thermal aging and fungal biodegradation on the oxidation and biodegradation of linear low density poly(ethylene) PE-LLD films containing Pro-Oxidant were examined. To achieve oxidation and degradation, films were first exposed to the sunlight for 93 days during the summer months followed by their incubation with fungal strains previously isolated from the soil based on the ability to grow on the oxidized PE-LLD as a sole carbon source. Some films were also thermally aged at temperatures ranging between 45°C and 65 °C, either before or after fungal degradation. Films with Pro-Oxidant additives exhibited a higher level of oxidation as revealed by increase in their carbonyl index (CO i ). In addition to increase in the CO i , films showed a slight increase in crystallinity and melting temperature ( T m ), considerably lower onset degradation temperatures, and a concomitant increase in the % weight of the residues. The level of oxidation observed in thermally aged films was directly proportional to the aging temperature. The PE-LLD films with Pro-Oxidant exposed to sunlight followed by thermal aging showed even higher rate and extent of oxidation when subsequently subjected to fungal biodegradation. The higher oxidation rate also correlated well with the CO 2 production in the fungal biodegradation tests. Similar films oxidized and aged but not exposed to fungal biodegradation showed much less degradation. Microscopic examination showed a profuse growth and colonization of fungal mycelia on the oxidized films by one strain, while another spore-producing strain grew around the film edges. Data presented here suggest that abiotic oxidation of polymer's carbon backbone produced metabolites which supported metabolic activities in fungal cells leading to further biotically-mediated polymer degradation. Thus, a combined impact of abiotic and biotic factors promoted the oxidation/biodegradation of PE-LLD films containing Pro-Oxidants.
Hai Chen - One of the best experts on this subject based on the ideXlab platform.
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oxidative stress in ischemic brain damage mechanisms of cell death and potential molecular targets for neuroprotection
Antioxidants & Redox Signaling, 2011Co-Authors: Hai Chen, Hideyuki Yoshioka, Joo Eun Jung, Nobuya Okami, Hiroyuki Sakata, Carolina M Maier, Purnima Narasimhan, Christina E Goeders, Pak H ChanAbstract:Abstract Significant amounts of oxygen free radicals (oxidants) are generated during cerebral ischemia/reperfusion, and oxidative stress plays an important role in brain damage after stroke. In addition to oxidizing macromolecules, leading to cell injury, oxidants are also involved in cell death/survival signal pathways and cause mitochondrial dysfunction. Experimental data from laboratory animals that either overexpress (transgenic) or are deficient in (knock-out) antioxidant proteins, mainly superoxide dismutase, have provided strong evidence of the role of oxidative stress in ischemic brain damage. In addition to mitochondria, recent reports demonstrate that NADPH oxidase (NOX), an important Pro-Oxidant enzyme, is also involved in the generation of oxidants in the brain after stroke. Inhibition of NOX is neuroprotective against cerebral ischemia. We propose that superoxide dismutase and NOX activity in the brain is a major determinant for ischemic damage/repair and that these major anti- and pro-oxidan...
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oxidative stress in ischemic brain damage mechanisms of cell death and potential molecular targets for neuroprotection
Antioxidants & Redox Signaling, 2011Co-Authors: Hai Chen, Hideyuki Yoshioka, Joo Eun Jung, Nobuya Okami, Hiroyuki Sakata, Carolina M Maier, Purnima Narasimhan, Christina E Goeders, Gab Seok Kim, Pak H ChanAbstract:Abstract Significant amounts of oxygen free radicals (oxidants) are generated during cerebral ischemia/reperfusion, and oxidative stress plays an important role in brain damage after stroke. In addition to oxidizing macromolecules, leading to cell injury, oxidants are also involved in cell death/survival signal pathways and cause mitochondrial dysfunction. Experimental data from laboratory animals that either overexpress (transgenic) or are deficient in (knock-out) antioxidant proteins, mainly superoxide dismutase, have provided strong evidence of the role of oxidative stress in ischemic brain damage. In addition to mitochondria, recent reports demonstrate that NADPH oxidase (NOX), an important Pro-Oxidant enzyme, is also involved in the generation of oxidants in the brain after stroke. Inhibition of NOX is neuroprotective against cerebral ischemia. We propose that superoxide dismutase and NOX activity in the brain is a major determinant for ischemic damage/repair and that these major anti- and pro-oxidan...