PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27435875-4 2016 Superoxide dismutase 3 (Sod3), Gpx3, and Gpx activity were increased in mouse BALF during bleomycin-induced lung fibrosis. Bleomycin 90-99 superoxide dismutase 3, extracellular Mus musculus 0-22 31560857-0 2019 Redistribution of EC-SOD resolves bleomycin-induced inflammation via increased apoptosis of recruited alveolar macrophages. Bleomycin 34-43 superoxide dismutase 3, extracellular Mus musculus 18-24 32421439-0 2020 MicroRNA regulation post-bleomycin due to the R213G extracellular superoxide dismutase variant is predicted to suppress inflammatory and immune pathways. Bleomycin 25-34 superoxide dismutase 3, extracellular Mus musculus 52-86 32421439-2 2020 A naturally occurring single nucleotide polymorphism in the key extracellular antioxidant enzyme, extracellular superoxide dismutase (EC-SOD), results in an arginine to glycine substitution (R213G) which promotes resolution of inflammation and protection against bleomycin-induced ALI. Bleomycin 263-272 superoxide dismutase 3, extracellular Mus musculus 98-132 32421439-2 2020 A naturally occurring single nucleotide polymorphism in the key extracellular antioxidant enzyme, extracellular superoxide dismutase (EC-SOD), results in an arginine to glycine substitution (R213G) which promotes resolution of inflammation and protection against bleomycin-induced ALI. Bleomycin 263-272 superoxide dismutase 3, extracellular Mus musculus 134-140 32421439-3 2020 Previously we found that mice harboring the R213G mutation in EC-SOD exhibit a transcriptomic profile consistent with a striking suppression of inflammatory and immune pathways 7 days post-bleomycin. Bleomycin 189-198 superoxide dismutase 3, extracellular Mus musculus 62-68 30004839-0 2018 R213G polymorphism in SOD3 protects against bleomycin-induced inflammation and attenuates induction of proinflammatory pathways. Bleomycin 44-53 superoxide dismutase 3, extracellular Mus musculus 22-26 27805412-3 2017 We used R213G mice expressing a naturally occurring single-nucleotide polymorphism, rs1799895, within the heparin-binding domain of SOD3, which results in an amino acid substitution at position 213 to test the hypothesis that the redistribution of SOD3 into the extracellular fluids would impart protection against bleomycin-induced lung fibrosis and secondary pulmonary hypertension (PH). Bleomycin 315-324 superoxide dismutase 3, extracellular Mus musculus 132-136 27805412-4 2017 In R213G mice, SOD3 content and activity was increased in extracellular fluids and decreased in lung at baseline, with greater increases in bronchoalveolar lavage fluid (BALF) SOD3 compared with wild-type mice 3 days after bleomycin. Bleomycin 223-232 superoxide dismutase 3, extracellular Mus musculus 15-19 27805412-9 2017 We conclude that the redistribution of SOD3 as a result of the R213G single-nucleotide polymorphism protects mice from bleomycin-induced fibrosis and secondary PH by improved resolution of alveolar inflammation. Bleomycin 119-128 superoxide dismutase 3, extracellular Mus musculus 39-43 27435875-4 2016 Superoxide dismutase 3 (Sod3), Gpx3, and Gpx activity were increased in mouse BALF during bleomycin-induced lung fibrosis. Bleomycin 90-99 superoxide dismutase 3, extracellular Mus musculus 24-28 26322414-0 2015 Lack of EC-SOD worsens alveolar and vascular development in a neonatal mouse model of bleomycin-induced bronchopulmonary dysplasia and pulmonary hypertension. Bleomycin 86-95 superoxide dismutase 3, extracellular Mus musculus 8-14 26322414-10 2015 CONCLUSION: EC-SOD is critical in preserving normal lung development and loss of EC-SOD results in disrupted alveolar development, PAH and vascular remodeling at baseline, which is further worsened with bleomycin and associated with decreased activation of VEGFR2. Bleomycin 203-212 superoxide dismutase 3, extracellular Mus musculus 12-18 20539010-0 2011 Lung extracellular superoxide dismutase overexpression lessens bleomycin-induced pulmonary hypertension and vascular remodeling. Bleomycin 63-72 superoxide dismutase 3, extracellular Mus musculus 5-39 20539010-3 2011 We used a model of pulmonary hypertension secondary to bleomycin-induced pulmonary fibrosis to test the hypothesis that an imbalance in extracellular superoxide and its antioxidant defense, extracellular superoxide dismutase, will promote pulmonary vascular remodeling and pulmonary hypertension. Bleomycin 55-64 superoxide dismutase 3, extracellular Mus musculus 190-224 20539010-4 2011 We exposed transgenic mice overexpressing lung extracellular superoxide dismutase and wild-type littermates to a single dose of intratracheal bleomycin, and evaluated the mice weekly for up to 35 days. Bleomycin 142-151 superoxide dismutase 3, extracellular Mus musculus 47-81 20539010-6 2011 The overexpression of extracellular superoxide dismutase protected against late remodeling within the medial, adventitial, and intimal layers of the vessel wall after the administration of bleomycin, and attenuated pulmonary hypertension at the same late time point. Bleomycin 189-198 superoxide dismutase 3, extracellular Mus musculus 22-56 20539010-8 2011 The overexpression of extracellular superoxide dismutase attenuated late pulmonary hypertension and significantly improved survival after exposure to bleomycin. Bleomycin 150-159 superoxide dismutase 3, extracellular Mus musculus 22-56 20493858-0 2010 Extracellular superoxide dismutase attenuates release of pulmonary hyaluronan from the extracellular matrix following bleomycin exposure. Bleomycin 118-127 superoxide dismutase 3, extracellular Mus musculus 0-34 20493858-2 2010 It has been previously shown that EC-SOD knock-out mice are more susceptible to bleomycin-induced lung injury, however, the molecular mechanism(s) remains unclear. Bleomycin 80-89 superoxide dismutase 3, extracellular Mus musculus 34-40 20493858-3 2010 We report here that bleomycin-induced lung damage, in EC-SOD KO mice, is associated with increased hyaluronan release into alveolar fluid. Bleomycin 20-29 superoxide dismutase 3, extracellular Mus musculus 54-60 20493858-5 2010 Our results indicate that EC-SOD attenuates bleomycin-induced pulmonary injury, at least in part, by preventing superoxide-mediated release of hyaluronan into alveolar space. Bleomycin 44-53 superoxide dismutase 3, extracellular Mus musculus 26-32 19073610-13 2009 Syndecan-1 is also significantly elevated in the lavage fluid of EC-SOD-null mice after asbestos and bleomycin exposure. Bleomycin 101-110 superoxide dismutase 3, extracellular Mus musculus 65-71 11705698-0 2001 Altered expression of extracellular superoxide dismutase in mouse lung after bleomycin treatment. Bleomycin 77-86 superoxide dismutase 3, extracellular Mus musculus 22-56 14583340-0 2003 Enhanced bleomycin-induced pulmonary damage in mice lacking extracellular superoxide dismutase. Bleomycin 9-18 superoxide dismutase 3, extracellular Mus musculus 60-94 14583340-4 2003 Mice null for ec-sod display a marked increase in lung inflammation at 14 d post-bleomycin treatment as compared to their wild-type counterparts. Bleomycin 81-90 superoxide dismutase 3, extracellular Mus musculus 14-20 14583340-7 2003 2-Pyrrolidone levels in the lung hydrolysates from ec-sod null mice were increased at both 7 and 14 d post-bleomycin treatment as compared to wild-type mice, indicating EC-SOD can inhibit oxidative fragmentation of proteins in this specific model of oxidative stress. Bleomycin 107-116 superoxide dismutase 3, extracellular Mus musculus 51-57 14583340-7 2003 2-Pyrrolidone levels in the lung hydrolysates from ec-sod null mice were increased at both 7 and 14 d post-bleomycin treatment as compared to wild-type mice, indicating EC-SOD can inhibit oxidative fragmentation of proteins in this specific model of oxidative stress. Bleomycin 107-116 superoxide dismutase 3, extracellular Mus musculus 169-175 18165226-3 2008 Previous studies indicate that EC-SOD protects the lung in both bleomycin- and asbestos-induced models of pulmonary fibrosis. Bleomycin 64-73 superoxide dismutase 3, extracellular Mus musculus 31-37 16224105-10 2006 We also demonstrate that EC-SOD knockout mice possess greater lung inflammation in response to bleomycin and bacteria when compared with wild types. Bleomycin 95-104 superoxide dismutase 3, extracellular Mus musculus 25-31 15298984-3 2004 Extracellular superoxide dismutase (EC-SOD) is an antioxidant enzyme that protects the lung in a bleomycin-induced pulmonary fibrosis model, but its role has not been studied in asbestos-mediated disease. Bleomycin 97-106 superoxide dismutase 3, extracellular Mus musculus 0-34 15298984-3 2004 Extracellular superoxide dismutase (EC-SOD) is an antioxidant enzyme that protects the lung in a bleomycin-induced pulmonary fibrosis model, but its role has not been studied in asbestos-mediated disease. Bleomycin 97-106 superoxide dismutase 3, extracellular Mus musculus 36-42 11880297-0 2002 Role of extracellular superoxide dismutase in bleomycin-induced pulmonary fibrosis. Bleomycin 46-55 superoxide dismutase 3, extracellular Mus musculus 8-42 11880297-4 2002 We hypothesized that EC-SOD plays an important role in attenuating bleomycin-induced lung injury. Bleomycin 67-76 superoxide dismutase 3, extracellular Mus musculus 21-27 11880297-7 2002 Using mice that overexpress EC-SOD specifically in the lung, we found a 53 +/- 14% reduction in bleomycin-induced lung injury assessed histologically and a 17 +/- 6% reduction in lung collagen content 2 wk after bleomycin administration. Bleomycin 96-105 superoxide dismutase 3, extracellular Mus musculus 28-34 11880297-7 2002 Using mice that overexpress EC-SOD specifically in the lung, we found a 53 +/- 14% reduction in bleomycin-induced lung injury assessed histologically and a 17 +/- 6% reduction in lung collagen content 2 wk after bleomycin administration. Bleomycin 212-221 superoxide dismutase 3, extracellular Mus musculus 28-34 11880297-8 2002 We conclude that EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration. Bleomycin 128-137 superoxide dismutase 3, extracellular Mus musculus 17-23 11705698-7 2001 Notably, at 7 d post-treatment, the truncated form of EC-SOD was found in the bronchoalveolar lavage fluid of bleomycin-treated mice, suggesting that EC-SOD is being removed from the extracellular matrix through proteolysis. Bleomycin 110-119 superoxide dismutase 3, extracellular Mus musculus 54-60 11705698-7 2001 Notably, at 7 d post-treatment, the truncated form of EC-SOD was found in the bronchoalveolar lavage fluid of bleomycin-treated mice, suggesting that EC-SOD is being removed from the extracellular matrix through proteolysis. Bleomycin 110-119 superoxide dismutase 3, extracellular Mus musculus 150-156