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Smoking is a well\u2010known risk factor that increases vasospasm. However, the molecular mechanisms by which smoking leads to vasospasm and cardiovascular disease are not fully understood. This study was designed to examine whether <jats:styled-content style=\"fixed-case\">DMSO<\/jats:styled-content>\u2010extracted cigarette smoke particles (<jats:styled-content style=\"fixed-case\">DSP<\/jats:styled-content>) could induce up\u2010regulation of vascular endothelin type A (<jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content>) receptors, and whether <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor is up\u2010regulated through activation of extracellular regulated protein kinases 1 and 2 (<jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2) signal pathways. Mesenteric arterial segments from rats were cultured in the presence of <jats:styled-content style=\"fixed-case\">DSP<\/jats:styled-content>, water\u2010extracted cigarette smoke particles (<jats:styled-content style=\"fixed-case\">WSP<\/jats:styled-content>) or equivalent concentration of nicotine for up to 24 hr. The results showed that <jats:styled-content style=\"fixed-case\">DSP<\/jats:styled-content>, but not <jats:styled-content style=\"fixed-case\">WSP<\/jats:styled-content> or nicotine, induced <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor up\u2010regulation with increased <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor\u2010mediated contraction (myograph, <jats:italic>p<\/jats:italic> &lt; 0.001). Simultaneously, the expression of <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> (real\u2010time <jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>,<jats:italic> p<\/jats:italic> &lt; 0.001) and protein (immunohistochemistry) were enhanced in the smooth muscle cells, suggesting that the lipid\u2010soluble substances contained in cigarette smoke were responsible for the effects of <jats:styled-content style=\"fixed-case\">DSP<\/jats:styled-content>. Actinomycin D (a general transcriptional inhibitor) decreased <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression and attenuated receptor\u2010mediated contraction (<jats:italic>p<\/jats:italic> &lt; 0.001), while <jats:styled-content style=\"fixed-case\">DSP<\/jats:styled-content> accelerated <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> degradation (<jats:italic>p<\/jats:italic> &lt; 0.01) and promoted the translation of <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> into protein. Furthermore, the up\u2010regulation of <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptors was significantly attenuated by inhibition of <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2 signal pathways (<jats:italic>p<\/jats:italic> &lt; 0.001). In conclusion, <jats:styled-content style=\"fixed-case\">DSP<\/jats:styled-content> most likely activate <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2 signal pathway\u2010mediated transcriptional and post\u2010transcriptional (translational) mechanisms that lead to vascular <jats:styled-content style=\"fixed-case\">ET<jats:sub>A<\/jats:sub><\/jats:styled-content> receptor up\u2010regulation, which might contribute to vasospasm and the development of smoking\u2010associated cardiovascular diseases.<\/jats:p>","DOI":"10.1111\/bcpt.12688","type":"journal-article","created":{"date-parts":[[2016,10,13]],"date-time":"2016-10-13T20:43:02Z","timestamp":1476391382000},"page":"327-334","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Lipid\u2010soluble Cigarette Smoke Particles Induced Vascular Endothelin Type A Receptor Up\u2010Regulation through Activation of <scp>ERK<\/scp>1\/2 Signal Pathways"],"prefix":"10.1111","volume":"120","author":[{"given":"Yaping","family":"Zhang","sequence":"first","affiliation":[{"name":"Shaanxi Key Laboratory of Ischemic Cardiovascular Disease Institute of Basic and Translational Medicine Xi'an Medical University Xi'an China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Experimental Vascular Research Institute of Clinical Science in Lund Lund University Lund Sweden"},{"name":"Xiamen Institute of Cardiovascular Diseases The First Affiliated Hospital of Xiamen University Xiamen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars","family":"Edvinsson","sequence":"additional","affiliation":[{"name":"Division of Experimental Vascular Research Institute of Clinical Science in Lund Lund University Lund Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cang\u2010Bao","family":"Xu","sequence":"additional","affiliation":[{"name":"Shaanxi Key Laboratory of Ischemic Cardiovascular Disease Institute of Basic and Translational Medicine Xi'an Medical University Xi'an China"},{"name":"Division of Experimental Vascular Research Institute of Clinical Science in Lund Lund University Lund 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