http://purl.uniprot.org/citations/22994521 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/22994521 | http://www.w3.org/2000/01/rdf-schema#comment | "Chronic hypoxia (CH) induces an inflammatory response in rat carotid body that is characterized by immune cell invasion and the expression of pro-inflammatory cytokines. In the present study, we have investigated the role of type-A endothelin (ET-A) receptors in the development of CH-induced inflammation. After 7 days of CH (380 Torr), double-label immunofluorescence studies demonstrated elevated levels of ET-A receptor and tyrosine hydroxylase (TH) in O(2)-sensitive type I cells. Following CH, ET-A receptors were also expressed on resident and invasive CD45+ immune cells distributed in tissue surrounding chemosensory cell lobules. Immnofluorescence and quantitative PCR studies showed that concurrent treatment with the ET-A/B receptor antagonist, bosentan (200 mg/kg/day), blocked CH-induced ED-1+ macrophage invasion and the upregulation of cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor α (TNFα), and monocyte chemoattractant protein-1 (MCP-1). Moreover, bosentan treatment blocked the CH-induced increases in expression of acid-sensitive ion channels (ASICs) in chemoafferent neurons in the petrosal ganglion (PG). Our findings are consistent with the hypothesis that CH-induced inflammation involves the upregulation and release of ET-1 from type I cells. ET-1 may act in an autocrine/paracrine mechanism via ET-A receptors on chemosensory type I cells and immune cells to promote an inflammatory response."xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.org/dc/terms/identifier | "doi:10.1089/ham.2012.1011"xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/author | "He L."xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/author | "Dinger B."xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/author | "Fidone S."xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/author | "Stensaas L."xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/name | "High Alt Med Biol"xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/pages | "209-216"xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/title | "Effect of endothelin receptor antagonist bosentan on chronic hypoxia-induced inflammation and chemoafferent neuron adaptation in rat carotid body."xsd:string |
http://purl.uniprot.org/citations/22994521 | http://purl.uniprot.org/core/volume | "13"xsd:string |
http://purl.uniprot.org/citations/22994521 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22994521 |
http://purl.uniprot.org/citations/22994521 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/22994521 |
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http://purl.uniprot.org/uniprot/#_Q5BKB0-mappedCitation-22994521 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22994521 |
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http://purl.uniprot.org/uniprot/Q63264 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/22994521 |
http://purl.uniprot.org/uniprot/A0A8I6A5V4 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/22994521 |
http://purl.uniprot.org/uniprot/Q5BKB0 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/22994521 |