PMC:3317373 / 15826-16891 JSONTXT

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As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T7325","span":{"begin":790,"end":795},"obj":"Protein"},{"id":"T7324","span":{"begin":734,"end":738},"obj":"Protein"},{"id":"T7323","span":{"begin":703,"end":707},"obj":"Protein"},{"id":"T7322","span":{"begin":670,"end":674},"obj":"Protein"},{"id":"T7321","span":{"begin":637,"end":642},"obj":"Protein"},{"id":"T7320","span":{"begin":437,"end":441},"obj":"Protein"},{"id":"T7319","span":{"begin":278,"end":282},"obj":"Protein"},{"id":"T7318","span":{"begin":267,"end":272},"obj":"Protein"},{"id":"T7317","span":{"begin":201,"end":205},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T8387","span":{"begin":694,"end":705},"obj":"http://www.uniprot.org/uniprot/P35225"},{"id":"T8382","span":{"begin":703,"end":707},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T8381","span":{"begin":278,"end":282},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T8375","span":{"begin":790,"end":795},"obj":"http://www.uniprot.org/uniprot/P01584"},{"id":"T8374","span":{"begin":637,"end":642},"obj":"http://www.uniprot.org/uniprot/P01584"},{"id":"T8373","span":{"begin":267,"end":272},"obj":"http://www.uniprot.org/uniprot/P01584"},{"id":"T8367","span":{"begin":780,"end":785},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T8366","span":{"begin":627,"end":632},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T8365","span":{"begin":260,"end":265},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T8360","span":{"begin":780,"end":783},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T8359","span":{"begin":627,"end":630},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T8358","span":{"begin":260,"end":263},"obj":"http://www.uniprot.org/uniprot/P01375"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"UBERON-AE","denotations":[{"id":"T7206","span":{"begin":748,"end":753},"obj":"http://purl.obolibrary.org/obo/UBERON_0001155"},{"id":"T7204","span":{"begin":293,"end":300},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"T7203","span":{"begin":62,"end":73},"obj":"http://purl.obolibrary.org/obo/UBERON_0002240"},{"id":"T7196","span":{"begin":956,"end":961},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T7195","span":{"begin":287,"end":292},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"T7194","span":{"begin":52,"end":57},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"GO-BP","denotations":[{"id":"T7349","span":{"begin":911,"end":923},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T7346","span":{"begin":184,"end":197},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T7343","span":{"begin":812,"end":831},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T7342","span":{"begin":30,"end":48},"obj":"http://purl.obolibrary.org/obo/GO_0051092"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"GO-MF","denotations":[{"id":"T8284","span":{"begin":703,"end":707},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T8283","span":{"begin":278,"end":282},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T8281","span":{"begin":401,"end":408},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T8279","span":{"begin":397,"end":408},"obj":"http://purl.obolibrary.org/obo/GO_0003677"},{"id":"T8290","span":{"begin":694,"end":705},"obj":"http://purl.obolibrary.org/obo/GO_0005144"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"GO-CC","denotations":[{"id":"T8296","span":{"begin":764,"end":769},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"sentences","denotations":[{"id":"T7222","span":{"begin":963,"end":1065},"obj":"Sentence"},{"id":"T7221","span":{"begin":842,"end":962},"obj":"Sentence"},{"id":"T7220","span":{"begin":614,"end":841},"obj":"Sentence"},{"id":"T7219","span":{"begin":513,"end":613},"obj":"Sentence"},{"id":"T7218","span":{"begin":324,"end":512},"obj":"Sentence"},{"id":"T7217","span":{"begin":105,"end":323},"obj":"Sentence"},{"id":"T7216","span":{"begin":0,"end":104},"obj":"Sentence"},{"id":"T162","span":{"begin":0,"end":104},"obj":"Sentence"},{"id":"T163","span":{"begin":105,"end":323},"obj":"Sentence"},{"id":"T164","span":{"begin":324,"end":512},"obj":"Sentence"},{"id":"T165","span":{"begin":513,"end":613},"obj":"Sentence"},{"id":"T166","span":{"begin":614,"end":841},"obj":"Sentence"},{"id":"T167","span":{"begin":842,"end":962},"obj":"Sentence"},{"id":"T168","span":{"begin":963,"end":1065},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"ICD10","denotations":[{"id":"T8272","span":{"begin":946,"end":952},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T8271","span":{"begin":363,"end":369},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"},{"id":"T8270","span":{"begin":90,"end":96},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"simple1","denotations":[{"id":"T8340","span":{"begin":790,"end":795},"obj":"Protein"},{"id":"T8339","span":{"begin":734,"end":738},"obj":"Protein"},{"id":"T8338","span":{"begin":703,"end":707},"obj":"Protein"},{"id":"T8337","span":{"begin":670,"end":674},"obj":"Protein"},{"id":"T8336","span":{"begin":637,"end":642},"obj":"Protein"},{"id":"T8335","span":{"begin":437,"end":441},"obj":"Protein"},{"id":"T8334","span":{"begin":278,"end":282},"obj":"Protein"},{"id":"T8333","span":{"begin":267,"end":272},"obj":"Protein"},{"id":"T8332","span":{"begin":201,"end":205},"obj":"Protein"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"BioNLP16_DUT","denotations":[{"id":"T9924","span":{"begin":716,"end":730},"obj":"Positive_regulation"},{"id":"T9923","span":{"begin":708,"end":715},"obj":"Positive_regulation"},{"id":"T9922","span":{"begin":419,"end":433},"obj":"Positive_regulation"},{"id":"T9921","span":{"begin":419,"end":433},"obj":"Gene_expression"},{"id":"T9920","span":{"begin":176,"end":183},"obj":"Positive_regulation"},{"id":"T9919","span":{"begin":184,"end":197},"obj":"Transcription"},{"id":"T9899","span":{"begin":670,"end":674},"obj":"Protein"},{"id":"T9898","span":{"begin":637,"end":642},"obj":"Protein"},{"id":"T9897","span":{"begin":790,"end":795},"obj":"Protein"},{"id":"T9896","span":{"begin":734,"end":738},"obj":"Protein"},{"id":"T9895","span":{"begin":703,"end":707},"obj":"Protein"},{"id":"T9894","span":{"begin":437,"end":441},"obj":"Protein"},{"id":"T9893","span":{"begin":278,"end":282},"obj":"Protein"},{"id":"T9892","span":{"begin":267,"end":272},"obj":"Protein"},{"id":"T9891","span":{"begin":201,"end":205},"obj":"Protein"}],"relations":[{"id":"R8154","pred":"themeOf","subj":"T9891","obj":"T9919"},{"id":"R8156","pred":"themeOf","subj":"T9894","obj":"T9921"},{"id":"R8158","pred":"themeOf","subj":"T9896","obj":"T9924"},{"id":"R8176","pred":"themeOf","subj":"T9919","obj":"T9920"},{"id":"R8177","pred":"themeOf","subj":"T9921","obj":"T9922"},{"id":"R8181","pred":"themeOf","subj":"T9924","obj":"T9923"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

{"project":"BioNLP16_Messiy","denotations":[{"id":"T8479","span":{"begin":708,"end":715},"obj":"Positive_regulation"},{"id":"T8478","span":{"begin":716,"end":730},"obj":"Positive_regulation"},{"id":"T8477","span":{"begin":419,"end":433},"obj":"Positive_regulation"},{"id":"T8476","span":{"begin":370,"end":377},"obj":"Positive_regulation"},{"id":"T8475","span":{"begin":176,"end":183},"obj":"Positive_regulation"},{"id":"T8474","span":{"begin":184,"end":197},"obj":"Transcription"},{"id":"T8454","span":{"begin":637,"end":642},"obj":"Protein"},{"id":"T8453","span":{"begin":790,"end":795},"obj":"Protein"},{"id":"T8452","span":{"begin":734,"end":738},"obj":"Protein"},{"id":"T8451","span":{"begin":703,"end":707},"obj":"Protein"},{"id":"T8450","span":{"begin":437,"end":441},"obj":"Protein"},{"id":"T8449","span":{"begin":278,"end":282},"obj":"Protein"},{"id":"T8448","span":{"begin":267,"end":272},"obj":"Protein"},{"id":"T8447","span":{"begin":201,"end":205},"obj":"Protein"},{"id":"T8455","span":{"begin":670,"end":674},"obj":"Protein"}],"relations":[{"id":"R6872","pred":"themeOf","subj":"T8447","obj":"T8474"},{"id":"R6873","pred":"themeOf","subj":"T8450","obj":"T8477"},{"id":"R6874","pred":"themeOf","subj":"T8450","obj":"T8476"},{"id":"R6875","pred":"themeOf","subj":"T8452","obj":"T8478"},{"id":"R6898","pred":"themeOf","subj":"T8474","obj":"T8475"},{"id":"R6899","pred":"themeOf","subj":"T8478","obj":"T8479"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

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has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}

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{"project":"test3","denotations":[{"id":"T7119","span":{"begin":790,"end":795},"obj":"Protein"},{"id":"T7118","span":{"begin":734,"end":738},"obj":"Protein"},{"id":"T7117","span":{"begin":703,"end":707},"obj":"Protein"},{"id":"T7116","span":{"begin":670,"end":674},"obj":"Protein"},{"id":"T7115","span":{"begin":637,"end":642},"obj":"Protein"},{"id":"T7114","span":{"begin":437,"end":441},"obj":"Protein"},{"id":"T7113","span":{"begin":278,"end":282},"obj":"Protein"},{"id":"T7112","span":{"begin":267,"end":272},"obj":"Protein"},{"id":"T7111","span":{"begin":201,"end":205},"obj":"Protein"},{"id":"T7155","span":{"begin":790,"end":795},"obj":"Protein"},{"id":"T7154","span":{"begin":734,"end":738},"obj":"Protein"},{"id":"T7153","span":{"begin":716,"end":730},"obj":"Positive_regulation"},{"id":"T7152","span":{"begin":708,"end":715},"obj":"Positive_regulation"},{"id":"T7151","span":{"begin":703,"end":707},"obj":"Protein"},{"id":"T7150","span":{"begin":670,"end":674},"obj":"Protein"},{"id":"T7149","span":{"begin":637,"end":642},"obj":"Protein"},{"id":"T7148","span":{"begin":437,"end":441},"obj":"Protein"},{"id":"T7147","span":{"begin":419,"end":433},"obj":"Positive_regulation"},{"id":"T7146","span":{"begin":278,"end":282},"obj":"Protein"},{"id":"T7145","span":{"begin":267,"end":272},"obj":"Protein"},{"id":"T7144","span":{"begin":201,"end":205},"obj":"Protein"},{"id":"T7143","span":{"begin":184,"end":197},"obj":"Transcription"},{"id":"T7142","span":{"begin":176,"end":183},"obj":"Positive_regulation"}],"relations":[{"id":"R5840","pred":"themeOf","subj":"T7143","obj":"T7142"},{"id":"R5841","pred":"themeOf","subj":"T7144","obj":"T7143"},{"id":"R5842","pred":"themeOf","subj":"T7145","obj":"T7143"},{"id":"R5843","pred":"themeOf","subj":"T7146","obj":"T7143"},{"id":"R5844","pred":"themeOf","subj":"T7148","obj":"T7147"},{"id":"R5845","pred":"causeOf","subj":"T7151","obj":"T7152"},{"id":"R5846","pred":"themeOf","subj":"T7153","obj":"T7152"},{"id":"R5847","pred":"themeOf","subj":"T7154","obj":"T7153"}],"text":"It has been demonstrated that NF-κB is activated in brain and spinal cord after traumatic injury [2, 9]. As a transcript factor, NF-κB binds with DNA once it was activated and induces transcription of MMP9 and a battery of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, in brain tissues after TBI [3, 10, 11]. Our results also revealed that scratch injury induced elevation of NF-κB DNA binding activity, overexpression of MMP9, and proinflammatory mediators mentioned above in cultured astrocytes. It has been demonstrated that there is an autoregulatory loop among these proinflammatory mediators. For example, TNF-α and IL-1β are potent stimulators for MMP9 in astrocytes [12, 13], and IL-6 induces overexpression of MMP9 in human colon carcinoma cells [14], and TNF-α and IL-1β also can induce activation of NF-κB [15, 16]. This autoregulatory loop extremely aggravates the damaging effect of inflammation and induces secondary injury to brain. It is a good choice for targeting on an upstream factor to prevent such autoregulatory loop after TBI."}