PubMed:24719110 JSONTXT

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":101},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":102,"end":286},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":287,"end":451},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":452,"end":692},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":693,"end":820},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":821,"end":920},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":921,"end":1074},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":1075,"end":1219},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":101},"obj":"Sentence"},{"id":"T2","span":{"begin":102,"end":286},"obj":"Sentence"},{"id":"T3","span":{"begin":287,"end":451},"obj":"Sentence"},{"id":"T4","span":{"begin":452,"end":692},"obj":"Sentence"},{"id":"T5","span":{"begin":693,"end":820},"obj":"Sentence"},{"id":"T6","span":{"begin":821,"end":920},"obj":"Sentence"},{"id":"T7","span":{"begin":921,"end":1074},"obj":"Sentence"},{"id":"T8","span":{"begin":1075,"end":1219},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":477,"end":483},"obj":"gene:2740"},{"id":"T1","span":{"begin":594,"end":602},"obj":"disease:C0011847"},{"id":"T2","span":{"begin":477,"end":483},"obj":"gene:2740"},{"id":"T3","span":{"begin":594,"end":602},"obj":"disease:C0011849"},{"id":"T4","span":{"begin":493,"end":498},"obj":"gene:100125288"},{"id":"T5","span":{"begin":594,"end":602},"obj":"disease:C0011847"},{"id":"T6","span":{"begin":493,"end":498},"obj":"gene:100125288"},{"id":"T7","span":{"begin":594,"end":602},"obj":"disease:C0011849"},{"id":"T8","span":{"begin":493,"end":498},"obj":"gene:79813"},{"id":"T9","span":{"begin":594,"end":602},"obj":"disease:C0011847"},{"id":"T10","span":{"begin":493,"end":498},"obj":"gene:79813"},{"id":"T11","span":{"begin":594,"end":602},"obj":"disease:C0011849"},{"id":"T12","span":{"begin":493,"end":498},"obj":"gene:2641"},{"id":"T13","span":{"begin":594,"end":602},"obj":"disease:C0011847"},{"id":"T14","span":{"begin":493,"end":498},"obj":"gene:2641"},{"id":"T15","span":{"begin":594,"end":602},"obj":"disease:C0011849"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"},{"id":"R5","pred":"associated_with","subj":"T8","obj":"T9"},{"id":"R6","pred":"associated_with","subj":"T10","obj":"T11"},{"id":"R7","pred":"associated_with","subj":"T12","obj":"T13"},{"id":"R8","pred":"associated_with","subj":"T14","obj":"T15"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":219,"end":223},"obj":"HP_0012531"},{"id":"T2","span":{"begin":581,"end":587},"obj":"HP_0002664"},{"id":"T3","span":{"begin":1190,"end":1194},"obj":"HP_0012531"}],"text":"Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}

{"project":"Allie","denotations":[{"id":"SS1_24719110_1_0","span":{"begin":164,"end":196},"obj":"expanded"},{"id":"SS2_24719110_1_0","span":{"begin":198,"end":204},"obj":"abbr"}],"relations":[{"id":"AE1_24719110_1_0","pred":"abbreviatedTo","subj":"SS1_24719110_1_0","obj":"SS2_24719110_1_0"}],"text":"Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}

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of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T2712","span":{"begin":493,"end":498},"obj":"gene:79813"},{"id":"T2713","span":{"begin":594,"end":602},"obj":"disease:C0011847"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T2712","obj":"T2713"},{"id":"R2","pred":"associated_with","subj":"T2712","obj":"T2713"},{"id":"R3","pred":"associated_with","subj":"T2712","obj":"T2713"},{"id":"R4","pred":"associated_with","subj":"T2712","obj":"T2713"},{"id":"R5","pred":"associated_with","subj":"T2712","obj":"T2713"},{"id":"R6","pred":"associated_with","subj":"T2712","obj":"T2713"},{"id":"R7","pred":"associated_with","subj":"T2712","obj":"T2713"},{"id":"R8","pred":"associated_with","subj":"T2712","obj":"T2713"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}

{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":388,"end":392},"obj":"http://purl.obolibrary.org/obo/UBERON_0006967"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1120,"end":1124},"obj":"http://purl.obolibrary.org/obo/UBERON_0006967"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":438,"end":443},"obj":"http://purl.obolibrary.org/obo/UBERON_0001021"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":561,"end":566},"obj":"http://purl.obolibrary.org/obo/UBERON_0001021"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":885,"end":896},"obj":"http://purl.obolibrary.org/obo/UBERON_0002240"}],"text":"Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":438,"end":443},"obj":"http://purl.obolibrary.org/obo/UBERON_0001021"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":561,"end":566},"obj":"http://purl.obolibrary.org/obo/UBERON_0001021"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":388,"end":392},"obj":"http://purl.obolibrary.org/obo/UBERON_0006967"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1120,"end":1124},"obj":"http://purl.obolibrary.org/obo/UBERON_0006967"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":885,"end":896},"obj":"http://purl.obolibrary.org/obo/UBERON_0002240"}],"text":"Activation of spinal glucagon-like peptide-1 receptors specifically suppresses pain hypersensitivity.\nThis study aims to identify the inhibitory role of the spinal glucagon like peptide-1 receptor (GLP-1R) signaling in pain hypersensitivity and its mechanism of action in rats and mice. First, GLP-1Rs were identified to be specifically expressed on microglial cells in the spinal dorsal horn, and profoundly upregulated after peripheral nerve injury. In addition, intrathecal GLP-1R agonists GLP-1(7-36) and exenatide potently alleviated formalin-, peripheral nerve injury-, bone cancer-, and diabetes-induced hypersensitivity states by 60-90%, without affecting acute nociceptive responses. The antihypersensitive effects of exenatide and GLP-1 were completely prevented by GLP-1R antagonism and GLP-1R gene knockdown. Furthermore, exenatide evoked β-endorphin release from both the spinal cord and cultured microglia. Exenatide antiallodynia was completely prevented by the microglial inhibitor minocycline, β-endorphin antiserum, and opioid receptor antagonist naloxone. Our results illustrate a novel spinal dorsal horn microglial GLP-1R/β-endorphin inhibitory pathway in a variety of pain hypersensitivity states."}