PMC:7560808 / 10877-12076 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T58","span":{"begin":292,"end":300},"obj":"Body_part"},{"id":"T59","span":{"begin":336,"end":341},"obj":"Body_part"},{"id":"T60","span":{"begin":404,"end":426},"obj":"Body_part"},{"id":"T61","span":{"begin":577,"end":582},"obj":"Body_part"},{"id":"T62","span":{"begin":723,"end":725},"obj":"Body_part"},{"id":"T63","span":{"begin":776,"end":783},"obj":"Body_part"},{"id":"T64","span":{"begin":953,"end":958},"obj":"Body_part"}],"attributes":[{"id":"A58","pred":"fma_id","subj":"T58","obj":"http://purl.org/sig/ont/fma/fma63021"},{"id":"A59","pred":"fma_id","subj":"T59","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A60","pred":"fma_id","subj":"T60","obj":"http://purl.org/sig/ont/fma/fma67858"},{"id":"A61","pred":"fma_id","subj":"T61","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A62","pred":"fma_id","subj":"T62","obj":"http://purl.org/sig/ont/fma/fma63023"},{"id":"A63","pred":"fma_id","subj":"T63","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A64","pred":"fma_id","subj":"T64","obj":"http://purl.org/sig/ont/fma/fma63083"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T21","span":{"begin":228,"end":238},"obj":"Body_part"},{"id":"T22","span":{"begin":336,"end":341},"obj":"Body_part"},{"id":"T23","span":{"begin":577,"end":582},"obj":"Body_part"},{"id":"T24","span":{"begin":953,"end":958},"obj":"Body_part"}],"attributes":[{"id":"A21","pred":"uberon_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/UBERON_2001275"},{"id":"A22","pred":"uberon_id","subj":"T22","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A23","pred":"uberon_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A24","pred":"uberon_id","subj":"T24","obj":"http://purl.obolibrary.org/obo/UBERON_0001977"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T72","span":{"begin":21,"end":27},"obj":"Disease"},{"id":"T73","span":{"begin":143,"end":149},"obj":"Disease"},{"id":"T74","span":{"begin":160,"end":168},"obj":"Disease"},{"id":"T75","span":{"begin":877,"end":885},"obj":"Disease"},{"id":"T76","span":{"begin":944,"end":952},"obj":"Disease"},{"id":"T77","span":{"begin":1103,"end":1109},"obj":"Disease"},{"id":"T78","span":{"begin":1190,"end":1198},"obj":"Disease"}],"attributes":[{"id":"A72","pred":"mondo_id","subj":"T72","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A73","pred":"mondo_id","subj":"T73","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A74","pred":"mondo_id","subj":"T74","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A75","pred":"mondo_id","subj":"T75","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A76","pred":"mondo_id","subj":"T76","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A77","pred":"mondo_id","subj":"T77","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A78","pred":"mondo_id","subj":"T78","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T91","span":{"begin":79,"end":80},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T92","span":{"begin":336,"end":341},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T93","span":{"begin":336,"end":341},"obj":"http://www.ebi.ac.uk/efo/EFO_0000296"},{"id":"T94","span":{"begin":577,"end":582},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T95","span":{"begin":577,"end":582},"obj":"http://www.ebi.ac.uk/efo/EFO_0000296"},{"id":"T96","span":{"begin":687,"end":695},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T97","span":{"begin":771,"end":775},"obj":"http://purl.obolibrary.org/obo/CLO_0001236"},{"id":"T98","span":{"begin":789,"end":792},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T99","span":{"begin":811,"end":812},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T100","span":{"begin":982,"end":985},"obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"T101","span":{"begin":1078,"end":1079},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T48","span":{"begin":418,"end":426},"obj":"Chemical"},{"id":"T49","span":{"begin":723,"end":725},"obj":"Chemical"},{"id":"T51","span":{"begin":776,"end":783},"obj":"Chemical"},{"id":"T52","span":{"begin":824,"end":834},"obj":"Chemical"}],"attributes":[{"id":"A48","pred":"chebi_id","subj":"T48","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A49","pred":"chebi_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/CHEBI_74056"},{"id":"A50","pred":"chebi_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/CHEBI_28815"},{"id":"A51","pred":"chebi_id","subj":"T51","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A52","pred":"chebi_id","subj":"T52","obj":"http://purl.obolibrary.org/obo/CHEBI_48706"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T7","span":{"begin":726,"end":737},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T8","span":{"begin":900,"end":911},"obj":"http://purl.obolibrary.org/obo/GO_0009056"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-sentences","denotations":[{"id":"T121","span":{"begin":0,"end":169},"obj":"Sentence"},{"id":"T122","span":{"begin":170,"end":263},"obj":"Sentence"},{"id":"T123","span":{"begin":264,"end":515},"obj":"Sentence"},{"id":"T124","span":{"begin":516,"end":653},"obj":"Sentence"},{"id":"T125","span":{"begin":654,"end":886},"obj":"Sentence"},{"id":"T126","span":{"begin":887,"end":1007},"obj":"Sentence"},{"id":"T127","span":{"begin":1008,"end":1199},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PD-GlycoEpitope","denotations":[{"id":"T10","span":{"begin":723,"end":725},"obj":"GlycoEpitope"}],"attributes":[{"id":"A10","pred":"glyco_epitope_db_id","subj":"T10","obj":"http://www.glycoepitope.jp/epitopes/EP0086"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T11","span":{"begin":1163,"end":1186},"obj":"Phenotype"}],"attributes":[{"id":"A11","pred":"hp_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/HP_0032654"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}

{"project":"LitCovid-PubTator","denotations":[{"id":"296","span":{"begin":292,"end":302},"obj":"Gene"},{"id":"297","span":{"begin":663,"end":668},"obj":"Gene"},{"id":"298","span":{"begin":767,"end":772},"obj":"Gene"},{"id":"299","span":{"begin":838,"end":843},"obj":"Gene"},{"id":"300","span":{"begin":1001,"end":1006},"obj":"Gene"},{"id":"301","span":{"begin":254,"end":262},"obj":"Species"},{"id":"302","span":{"begin":351,"end":359},"obj":"Species"},{"id":"303","span":{"begin":569,"end":576},"obj":"Species"},{"id":"304","span":{"begin":178,"end":181},"obj":"Chemical"},{"id":"305","span":{"begin":239,"end":242},"obj":"Chemical"},{"id":"306","span":{"begin":919,"end":922},"obj":"Chemical"},{"id":"307","span":{"begin":1117,"end":1120},"obj":"Chemical"},{"id":"308","span":{"begin":131,"end":149},"obj":"Disease"},{"id":"309","span":{"begin":160,"end":168},"obj":"Disease"},{"id":"310","span":{"begin":877,"end":885},"obj":"Disease"},{"id":"311","span":{"begin":944,"end":952},"obj":"Disease"},{"id":"312","span":{"begin":1045,"end":1061},"obj":"Disease"},{"id":"313","span":{"begin":1190,"end":1198},"obj":"Disease"}],"attributes":[{"id":"A296","pred":"tao:has_database_id","subj":"296","obj":"Gene:6382"},{"id":"A297","pred":"tao:has_database_id","subj":"297","obj":"Gene:10855"},{"id":"A298","pred":"tao:has_database_id","subj":"298","obj":"Gene:60495"},{"id":"A299","pred":"tao:has_database_id","subj":"299","obj":"Gene:10855"},{"id":"A300","pred":"tao:has_database_id","subj":"300","obj":"Gene:60495"},{"id":"A301","pred":"tao:has_database_id","subj":"301","obj":"Tax:9606"},{"id":"A302","pred":"tao:has_database_id","subj":"302","obj":"Tax:9606"},{"id":"A303","pred":"tao:has_database_id","subj":"303","obj":"Tax:9606"},{"id":"A308","pred":"tao:has_database_id","subj":"308","obj":"MESH:D014947"},{"id":"A309","pred":"tao:has_database_id","subj":"309","obj":"MESH:C000657245"},{"id":"A310","pred":"tao:has_database_id","subj":"310","obj":"MESH:C000657245"},{"id":"A311","pred":"tao:has_database_id","subj":"311","obj":"MESH:C000657245"},{"id":"A312","pred":"tao:has_database_id","subj":"312","obj":"MESH:C000657245"},{"id":"A313","pred":"tao:has_database_id","subj":"313","obj":"MESH:C000657245"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"In summary, we found injury of the eGC and speculate that this might represent a potentially critical hallmark of later widespread endothelial injury in severe COVID-19. Reduced eGC thickness was visualized in vivo by employing sublingual SDF imaging in patients. At the same time, increased syndecan-1 and sTie-2 concentrations in the blood of these patients indicated shedding of important endothelial transmembrane proteins responsible for building (5) and maintaining (6) the structure of the eGC, respectively. Interestingly, eGC shedding could be reproduced when patient blood was transferred ex vivo into an endothelial microcapillary chip model. Although Hpa-1 and its enzymatic activity (primarily responsible for HS degradation) (7) was found to be normal, Hpa-2, a protein that has been described as a protective antagonist of Hpa-1 (8, 9), was severely depleted in COVID-19. Importantly, degradation of the eGC after perfusion with COVID-19 serum could be attenuated in ECs overexpressing Hpa-2. We therefore postulate that acquired Hpa-2 deficiency might represent a potential mechanism of injury to the eGC, which could later progress to widespread endothelial dysfunction in COVID-19."}