PubMed:18067895 JSONTXT

{"project":"sentences","denotations":[{"id":"TextSentencer_T8","span":{"begin":685,"end":751},"obj":"Sentence"},{"id":"TextSentencer_T1","span":{"begin":0,"end":99},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":100,"end":111},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":112,"end":251},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":252,"end":451},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":452,"end":460},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":461,"end":550},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":551,"end":684},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":752,"end":817},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":818,"end":853},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":854,"end":862},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":863,"end":969},"obj":"Sentence"},{"id":"TextSentencer_T13","span":{"begin":970,"end":1120},"obj":"Sentence"},{"id":"TextSentencer_T14","span":{"begin":1121,"end":1240},"obj":"Sentence"},{"id":"TextSentencer_T15","span":{"begin":1241,"end":1252},"obj":"Sentence"},{"id":"TextSentencer_T16","span":{"begin":1253,"end":1346},"obj":"Sentence"},{"id":"TextSentencer_T17","span":{"begin":1347,"end":1515},"obj":"Sentence"},{"id":"TextSentencer_T18","span":{"begin":1516,"end":1653},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":99},"obj":"Sentence"},{"id":"T2","span":{"begin":100,"end":111},"obj":"Sentence"},{"id":"T3","span":{"begin":112,"end":251},"obj":"Sentence"},{"id":"T4","span":{"begin":252,"end":451},"obj":"Sentence"},{"id":"T5","span":{"begin":452,"end":460},"obj":"Sentence"},{"id":"T6","span":{"begin":461,"end":550},"obj":"Sentence"},{"id":"T7","span":{"begin":551,"end":684},"obj":"Sentence"},{"id":"T8","span":{"begin":685,"end":751},"obj":"Sentence"},{"id":"T9","span":{"begin":752,"end":817},"obj":"Sentence"},{"id":"T10","span":{"begin":818,"end":853},"obj":"Sentence"},{"id":"T11","span":{"begin":854,"end":862},"obj":"Sentence"},{"id":"T12","span":{"begin":863,"end":969},"obj":"Sentence"},{"id":"T13","span":{"begin":970,"end":1120},"obj":"Sentence"},{"id":"T14","span":{"begin":1121,"end":1240},"obj":"Sentence"},{"id":"T15","span":{"begin":1241,"end":1252},"obj":"Sentence"},{"id":"T16","span":{"begin":1253,"end":1346},"obj":"Sentence"},{"id":"T17","span":{"begin":1347,"end":1515},"obj":"Sentence"},{"id":"T18","span":{"begin":1516,"end":1653},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"15-Lipoxygenase-2 expression in human macrophages induces chemokine secretion and T cell migration.\nBACKGROUND: We determined previously that hypoxia results in increased 15-lipoxygenase type 2 (15-LOX-2) expression and CXCL8 secretion in macrophages. This study sought to determine whether 15-LOX-2 expression links directly with the secretion of inflammatory molecules in macrophages and also investigated its subsequent effects on T cell migration.\nMETHODS: Adenovirus-mediated gene delivery caused overexpression of 15-LOX-2 in human macrophages. We used cytometric bead array to measure chemokine secretion, and assessed T cell migration by counting cells in chemotaxis chambers. Expression of chemokine receptors was determined by FACS analysis. Using siRNA, we reduced 15-LOX-2 expression in human macrophages. We used scrambled siRNA as control.\nRESULTS: Macrophages that overexpress 15-LOX-2 showed increased secretion of chemokine CXCL10 after 24h incubation. In addition, preconditioned medium from 15-LOX-2-overexpressing cells increased T cell migration and surface expression of CXCR3, the CXCL10 receptor. Knockdown of 15-LOX-2 expression decreased CXCL10 secretion from hypoxic macrophages and also reduced T cell migration.\nCONCLUSION: In macrophages, overexpression of 15-LOX-2 results in increased secretion of CXCL10 and CCL2. Products released in response to increased 15-LOX-2 activation lead to increased expression of CD69, the T cell activation marker as well as increased T cell migration. Therefore, increased expression of 15-LOX-2 induced by hypoxia may participate in T cell recruitment in diseases such as atherosclerosis."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":1551,"end":1559},"obj":"gene:247"},{"id":"T1","span":{"begin":1637,"end":1652},"obj":"disease:C0003850"},{"id":"T2","span":{"begin":1551,"end":1559},"obj":"gene:247"},{"id":"T3","span":{"begin":1637,"end":1652},"obj":"disease:C0004153"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"15-Lipoxygenase-2 expression in human macrophages induces chemokine secretion and T cell migration.\nBACKGROUND: We determined previously that hypoxia results in increased 15-lipoxygenase type 2 (15-LOX-2) expression and CXCL8 secretion in macrophages. This study sought to determine whether 15-LOX-2 expression links directly with the secretion of inflammatory molecules in macrophages and also investigated its subsequent effects on T cell migration.\nMETHODS: Adenovirus-mediated gene delivery caused overexpression of 15-LOX-2 in human macrophages. We used cytometric bead array to measure chemokine secretion, and assessed T cell migration by counting cells in chemotaxis chambers. Expression of chemokine receptors was determined by FACS analysis. Using siRNA, we reduced 15-LOX-2 expression in human macrophages. We used scrambled siRNA as control.\nRESULTS: Macrophages that overexpress 15-LOX-2 showed increased secretion of chemokine CXCL10 after 24h incubation. In addition, preconditioned medium from 15-LOX-2-overexpressing cells increased T cell migration and surface expression of CXCR3, the CXCL10 receptor. Knockdown of 15-LOX-2 expression decreased CXCL10 secretion from hypoxic macrophages and also reduced T cell migration.\nCONCLUSION: In macrophages, overexpression of 15-LOX-2 results in increased secretion of CXCL10 and CCL2. Products released in response to increased 15-LOX-2 activation lead to increased expression of CD69, the T cell activation marker as well as increased T cell migration. Therefore, increased expression of 15-LOX-2 induced by hypoxia may participate in T cell recruitment in diseases such as atherosclerosis."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"18067895-12#35#43#gene247","span":{"begin":1551,"end":1559},"obj":"gene247"},{"id":"18067895-12#121#136#diseaseC0003850","span":{"begin":1637,"end":1652},"obj":"diseaseC0003850"},{"id":"18067895-12#121#136#diseaseC0004153","span":{"begin":1637,"end":1652},"obj":"diseaseC0004153"}],"relations":[{"id":"35#43#gene247121#136#diseaseC0003850","pred":"associated_with","subj":"18067895-12#35#43#gene247","obj":"18067895-12#121#136#diseaseC0003850"},{"id":"35#43#gene247121#136#diseaseC0004153","pred":"associated_with","subj":"18067895-12#35#43#gene247","obj":"18067895-12#121#136#diseaseC0004153"}],"text":"15-Lipoxygenase-2 expression in human macrophages induces chemokine secretion and T cell migration.\nBACKGROUND: We determined previously that hypoxia results in increased 15-lipoxygenase type 2 (15-LOX-2) expression and CXCL8 secretion in macrophages. This study sought to determine whether 15-LOX-2 expression links directly with the secretion of inflammatory molecules in macrophages and also investigated its subsequent effects on T cell migration.\nMETHODS: Adenovirus-mediated gene delivery caused overexpression of 15-LOX-2 in human macrophages. We used cytometric bead array to measure chemokine secretion, and assessed T cell migration by counting cells in chemotaxis chambers. Expression of chemokine receptors was determined by FACS analysis. Using siRNA, we reduced 15-LOX-2 expression in human macrophages. We used scrambled siRNA as control.\nRESULTS: Macrophages that overexpress 15-LOX-2 showed increased secretion of chemokine CXCL10 after 24h incubation. In addition, preconditioned medium from 15-LOX-2-overexpressing cells increased T cell migration and surface expression of CXCR3, the CXCL10 receptor. Knockdown of 15-LOX-2 expression decreased CXCL10 secretion from hypoxic macrophages and also reduced T cell migration.\nCONCLUSION: In macrophages, overexpression of 15-LOX-2 results in increased secretion of CXCL10 and CCL2. Products released in response to increased 15-LOX-2 activation lead to increased expression of CD69, the T cell activation marker as well as increased T cell migration. Therefore, increased expression of 15-LOX-2 induced by hypoxia may participate in T cell recruitment in diseases such as atherosclerosis."}

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T862","span":{"begin":1551,"end":1559},"obj":"gene:247"},{"id":"T863","span":{"begin":1637,"end":1652},"obj":"disease:C0003850"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T862","obj":"T863"},{"id":"R2","pred":"associated_with","subj":"T862","obj":"T863"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"15-Lipoxygenase-2 expression in human macrophages induces chemokine secretion and T cell migration.\nBACKGROUND: We determined previously that hypoxia results in increased 15-lipoxygenase type 2 (15-LOX-2) expression and CXCL8 secretion in macrophages. This study sought to determine whether 15-LOX-2 expression links directly with the secretion of inflammatory molecules in macrophages and also investigated its subsequent effects on T cell migration.\nMETHODS: Adenovirus-mediated gene delivery caused overexpression of 15-LOX-2 in human macrophages. We used cytometric bead array to measure chemokine secretion, and assessed T cell migration by counting cells in chemotaxis chambers. Expression of chemokine receptors was determined by FACS analysis. Using siRNA, we reduced 15-LOX-2 expression in human macrophages. We used scrambled siRNA as control.\nRESULTS: Macrophages that overexpress 15-LOX-2 showed increased secretion of chemokine CXCL10 after 24h incubation. In addition, preconditioned medium from 15-LOX-2-overexpressing cells increased T cell migration and surface expression of CXCR3, the CXCL10 receptor. Knockdown of 15-LOX-2 expression decreased CXCL10 secretion from hypoxic macrophages and also reduced T cell migration.\nCONCLUSION: In macrophages, overexpression of 15-LOX-2 results in increased secretion of CXCL10 and CCL2. Products released in response to increased 15-LOX-2 activation lead to increased expression of CD69, the T cell activation marker as well as increased T cell migration. Therefore, increased expression of 15-LOX-2 induced by hypoxia may participate in T cell recruitment in diseases such as atherosclerosis."}