PubMed:15718492 JSONTXT

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":118},"obj":"Sentence"},{"id":"T2","span":{"begin":119,"end":130},"obj":"Sentence"},{"id":"T3","span":{"begin":131,"end":238},"obj":"Sentence"},{"id":"T4","span":{"begin":239,"end":373},"obj":"Sentence"},{"id":"T5","span":{"begin":374,"end":396},"obj":"Sentence"},{"id":"T6","span":{"begin":397,"end":646},"obj":"Sentence"},{"id":"T7","span":{"begin":647,"end":827},"obj":"Sentence"},{"id":"T8","span":{"begin":828,"end":1169},"obj":"Sentence"},{"id":"T9","span":{"begin":1170,"end":1297},"obj":"Sentence"},{"id":"T10","span":{"begin":1298,"end":1416},"obj":"Sentence"},{"id":"T11","span":{"begin":1417,"end":1429},"obj":"Sentence"},{"id":"T12","span":{"begin":1430,"end":1575},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":118},"obj":"Sentence"},{"id":"T2","span":{"begin":119,"end":130},"obj":"Sentence"},{"id":"T3","span":{"begin":131,"end":238},"obj":"Sentence"},{"id":"T4","span":{"begin":239,"end":373},"obj":"Sentence"},{"id":"T5","span":{"begin":374,"end":396},"obj":"Sentence"},{"id":"T6","span":{"begin":397,"end":646},"obj":"Sentence"},{"id":"T7","span":{"begin":647,"end":827},"obj":"Sentence"},{"id":"T8","span":{"begin":828,"end":1169},"obj":"Sentence"},{"id":"T9","span":{"begin":1170,"end":1297},"obj":"Sentence"},{"id":"T10","span":{"begin":1298,"end":1416},"obj":"Sentence"},{"id":"T11","span":{"begin":1417,"end":1429},"obj":"Sentence"},{"id":"T12","span":{"begin":1430,"end":1575},"obj":"Sentence"}],"text":"Shear stress inhibits smooth muscle cell-induced inflammatory gene expression in endothelial cells: role of NF-kappaB.\nOBJECTIVES: Vascular endothelial cells (ECs) are influenced by shear stress and neighboring smooth muscle cells (SMCs). We investigated the inflammation-relevant gene expression in EC/SMC cocultures under static condition and in response to shear stress.\nMATERIALS AND METHODS: Under static condition, DNA microarrays and reverse-transcription polymerase chain reaction identified 23 inflammation-relevant genes in ECs whose expression was significantly affected by coculture with SMCs, with 18 upregulated and 5 downregulated. Application of shear stress (12 dynes/cm2) to the EC side of the coculture for 6 hours inhibited most of the proinflammatory gene expressions in ECs induced by coculture with SMCs. Inhibition of nuclear factor-kappaB (NF-kappaB) activation by the p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced EC expression of proinflammatory genes, indicating that the NF-kappaB binding sites in the promoters of these genes play a significant role in their expression as a result of coculture with SMCs. Chromatin immunoprecipitation assays demonstrated the in vivo regulation of NF-kappaB recruitment to selected target promoters. Shear stress inhibited the SMC coculture-induced NF-kappaB activation in ECs and monocytic THP-1 cell adhesion to ECs.\nCONCLUSIONS: Our findings suggest that shear stress plays an inhibitory role in the proinflammatory gene expression in ECs located in close proximity to SMCs."}

{"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T1","span":{"begin":131,"end":373},"obj":"OBJECTIVE"},{"id":"T2","span":{"begin":397,"end":1416},"obj":"METHODS"},{"id":"T3","span":{"begin":1430,"end":1575},"obj":"CONCLUSIONS"}],"text":"Shear stress inhibits smooth muscle cell-induced inflammatory gene expression in endothelial cells: role of NF-kappaB.\nOBJECTIVES: Vascular endothelial cells (ECs) are influenced by shear stress and neighboring smooth muscle cells (SMCs). We investigated the inflammation-relevant gene expression in EC/SMC cocultures under static condition and in response to shear stress.\nMATERIALS AND METHODS: Under static condition, DNA microarrays and reverse-transcription polymerase chain reaction identified 23 inflammation-relevant genes in ECs whose expression was significantly affected by coculture with SMCs, with 18 upregulated and 5 downregulated. Application of shear stress (12 dynes/cm2) to the EC side of the coculture for 6 hours inhibited most of the proinflammatory gene expressions in ECs induced by coculture with SMCs. Inhibition of nuclear factor-kappaB (NF-kappaB) activation by the p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced EC expression of proinflammatory genes, indicating that the NF-kappaB binding sites in the promoters of these genes play a significant role in their expression as a result of coculture with SMCs. Chromatin immunoprecipitation assays demonstrated the in vivo regulation of NF-kappaB recruitment to selected target promoters. Shear stress inhibited the SMC coculture-induced NF-kappaB activation in ECs and monocytic THP-1 cell adhesion to ECs.\nCONCLUSIONS: Our findings suggest that shear stress plays an inhibitory role in the proinflammatory gene expression in ECs located in close proximity to SMCs."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":303,"end":306},"obj":"gene:54808"},{"id":"T1","span":{"begin":366,"end":372},"obj":"disease:C3825627"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Shear stress inhibits smooth muscle cell-induced inflammatory gene expression in endothelial cells: role of NF-kappaB.\nOBJECTIVES: Vascular endothelial cells (ECs) are influenced by shear stress and neighboring smooth muscle cells (SMCs). We investigated the inflammation-relevant gene expression in EC/SMC cocultures under static condition and in response to shear stress.\nMATERIALS AND METHODS: Under static condition, DNA microarrays and reverse-transcription polymerase chain reaction identified 23 inflammation-relevant genes in ECs whose expression was significantly affected by coculture with SMCs, with 18 upregulated and 5 downregulated. Application of shear stress (12 dynes/cm2) to the EC side of the coculture for 6 hours inhibited most of the proinflammatory gene expressions in ECs induced by coculture with SMCs. Inhibition of nuclear factor-kappaB (NF-kappaB) activation by the p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced EC expression of proinflammatory genes, indicating that the NF-kappaB binding sites in the promoters of these genes play a significant role in their expression as a result of coculture with SMCs. Chromatin immunoprecipitation assays demonstrated the in vivo regulation of NF-kappaB recruitment to selected target promoters. Shear stress inhibited the SMC coculture-induced NF-kappaB activation in ECs and monocytic THP-1 cell adhesion to ECs.\nCONCLUSIONS: Our findings suggest that shear stress plays an inhibitory role in the proinflammatory gene expression in ECs located in close proximity to SMCs."}