{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T13:00:39Z","timestamp":1773493239871,"version":"3.50.1"},"reference-count":81,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2013,3,13]],"date-time":"2013-03-13T00:00:00Z","timestamp":1363132800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Laryngoscope"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:sec><jats:title>Objectives\/Hypothesis<\/jats:title><jats:p>Nicotine, a major constituent of cigarette smoke, can activate the cholinergic anti\u2010inflammatory pathway by binding to \u03b17\u2010nicotinic acetylcholine receptor (\u03b17nAChR) expressed on the surface of certain cells. Here, we ask whether cigarette smoke extract induced different paracrine factors compared to the in vivo regulator of inflammation, tumor necrosis factor\u2010\u03b1, in human vocal fold fibroblasts (hVFFs) shown to express low levels of \u03b17nAChR.<\/jats:p><\/jats:sec><jats:sec><jats:title>Study Design<\/jats:title><jats:p>In vitro.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>\u03b17nAChR was detected by nested polymerase chain reaction and immunohistochemistry. \u03b3H2AX, a marker for DNA double\u2010stand breaks, was measured by immunofluorescence. Cigarette smoke extract was prepared in accordance with investigators studying effects of cigarette smoke. hVFFs treated for 3 hours had media replaced for an additional 24 hours. Cytokine, chemokine, and growth factor levels in media were assessed by multiplex analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>\u03b17nAChR expression levels decreased with the passage number of fibroblasts. Tumor necrosis factor\u2010\u03b1 induced a significantly different profile of cytokines, chemokines, and growth factor compared to cigarette smoke extract exposure. Cigarette smoke extract at a concentration not associated with induction of \u03b3H2AX nuclear foci significantly increased vascular endothelial growth factor.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Cigarette smoke extract elicited a response important for regulation of angiogenesis and vascular permeability during inflammation, without evidence of DNA double\u2010stand breaks associated with carcinogenesis. hVFFs are capable of participating in paracrine regulation of pathological blood vessel formation associated with cigarette smoking\u2013related diseases (ie, Reinke edema). These cells express \u03b17nAChR, an essential component of the cholinergic anti\u2010inflammatory pathway regulated by the vagus nerve in certain tissues and a target of therapeutic agents. <jats:italic>Laryngoscope<\/jats:italic>, 123:2228\u20132236, 2013<\/jats:p><\/jats:sec>","DOI":"10.1002\/lary.24052","type":"journal-article","created":{"date-parts":[[2013,3,14]],"date-time":"2013-03-14T09:40:40Z","timestamp":1363254040000},"page":"2228-2236","source":"Crossref","is-referenced-by-count":19,"title":["Paracrine potential of fibroblasts exposed to cigarette smoke extract with vascular growth factor induction"],"prefix":"10.1002","volume":"123","author":[{"given":"Craig M.","family":"Berchtold","sequence":"first","affiliation":[{"name":"Department of Surgery University of Wisconsin Madison Wisconsin U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adam","family":"Coughlin","sequence":"additional","affiliation":[{"name":"Department of Surgery University of 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