PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35488279-6 2022 In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent. Reactive Oxygen Species 80-103 hemolytic complement Mus musculus 34-37 35488279-6 2022 In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent. Reactive Oxygen Species 105-108 hemolytic complement Mus musculus 34-37 35488279-6 2022 In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent. Reactive Oxygen Species 175-178 hemolytic complement Mus musculus 34-37 35488279-6 2022 In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent. Reactive Oxygen Species 175-178 hemolytic complement Mus musculus 153-156 33858424-6 2021 RESULTS: To achieve this goal, a traditional nanoantioxidant of nanoceria was surface conjugated with the anti-C5a aptamers (Ceria@Apt) to scavenge the ROS and reduce C5a-mediated inflammation. Reactive Oxygen Species 152-155 hemolytic complement Mus musculus 111-114 35007559-7 2022 In vitro, C5ar2-/- neutrophils exhibited significantly reduced (Ca2+)i flux, reactive oxygen species release, and migratory capacity when activated with immune complexes or exposed to C5a. Reactive Oxygen Species 77-100 hemolytic complement Mus musculus 184-187 27543123-8 2016 In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent. Reactive Oxygen Species 123-146 hemolytic complement Mus musculus 50-53 28167912-7 2017 Mechanistic studies revealed that C5a most likely increased NLRP3 inflammasome activation via production of reactive oxygen species (ROS), and not through increased transcription of inflammasome components. Reactive Oxygen Species 108-131 hemolytic complement Mus musculus 34-37 28167912-7 2017 Mechanistic studies revealed that C5a most likely increased NLRP3 inflammasome activation via production of reactive oxygen species (ROS), and not through increased transcription of inflammasome components. Reactive Oxygen Species 133-136 hemolytic complement Mus musculus 34-37 28167912-8 2017 Therefore we conclude that C5a generated upon MSU-induced complement activation increases neutrophil recruitment in vivo by promoting IL-1 production via the generation of ROS, which activate the NLRP3 inflammasome. Reactive Oxygen Species 172-175 hemolytic complement Mus musculus 27-30 33852847-6 2021 Stimulation of C5aR+ LysoDCs by C5a increases reactive oxygen species levels, leading to efficient antigen cross-presentation, which elicits an antigen-specific CD8+ T cell response. Reactive Oxygen Species 46-69 hemolytic complement Mus musculus 15-18 32868671-4 2020 Macrophages have previously also been suggested to be pathogenic in mice via binding of C5a to their C5a-receptor, producing reactive oxygen species (ROS), which damages the pulmonary endothelium. Reactive Oxygen Species 125-148 hemolytic complement Mus musculus 88-113 32868671-4 2020 Macrophages have previously also been suggested to be pathogenic in mice via binding of C5a to their C5a-receptor, producing reactive oxygen species (ROS), which damages the pulmonary endothelium. Reactive Oxygen Species 150-153 hemolytic complement Mus musculus 88-113 31510052-8 2019 Reactive oxygen species (ROS) formation was detected in C5a-treated mouse KECs; however, W-54011 or NAC pretreatment inhibited high-dose rmC5a-induced ROS formation and also reduced cytochrome c release, apoptotic cell formation, and apoptotic DNA fragmentation. Reactive Oxygen Species 0-23 hemolytic complement Mus musculus 56-59 31510052-8 2019 Reactive oxygen species (ROS) formation was detected in C5a-treated mouse KECs; however, W-54011 or NAC pretreatment inhibited high-dose rmC5a-induced ROS formation and also reduced cytochrome c release, apoptotic cell formation, and apoptotic DNA fragmentation. Reactive Oxygen Species 25-28 hemolytic complement Mus musculus 56-59 31510052-9 2019 These factors determined the apoptosis of mouse KECs treated with high-dose C5a through C5aR and subsequently led to apoptosis via ROS regeneration and cytochrome c release. Reactive Oxygen Species 131-134 hemolytic complement Mus musculus 76-79 31510052-10 2019 The results showed that high concentrations of C5a induced mouse KEC apoptosis via a C5aR/ROS/mitochondria-dependent pathway. Reactive Oxygen Species 90-93 hemolytic complement Mus musculus 47-50 27543123-8 2016 In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent. Reactive Oxygen Species 123-146 hemolytic complement Mus musculus 56-59 27543123-8 2016 In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent. Reactive Oxygen Species 148-151 hemolytic complement Mus musculus 50-53 27543123-8 2016 In vitro exposure of wild-type CMs to recombinant C5a (rC5a) caused elevations in both cytosolic and nuclear/mitochondrial reactive oxygen species (ROS), which were C5a-receptor dependent. Reactive Oxygen Species 148-151 hemolytic complement Mus musculus 56-59