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The ubiquitously expressed <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> has been implicated in vascular remodelling preceding end\u2010organ damage by pharmacological inhibition, and <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content> signalling in cultured vascular cells is partly <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\u2010dependent. However, the role of <jats:styled-content style=\"fixed-case\">VSMC<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> in\u00a0vivo during <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content>\u2010induced pathophysiological processes is not known.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This study assesses the in\u00a0vivo relevance of <jats:styled-content style=\"fixed-case\">VSMC<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> during chronic <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content> challenge without further stressors, using a mouse model with inducible, <jats:styled-content style=\"fixed-case\">VSMC<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> knock out (<jats:styled-content style=\"fixed-case\">VSMC<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>). In these mice functional and structural vascular, renal and cardiac effects or biomarkers were investigated in\u00a0vivo and ex\u00a0vivo.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Vascular smooth muscle cell\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content> prevented <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content>\u2010induced media hypertrophy of mesenteric arteries, renal arterioles and the aorta, <jats:styled-content style=\"fixed-case\">VSMC ERK<\/jats:styled-content>1\/2\u2010phosphorylation as well as the impairment of vascular compliance. Furthermore, induction of vascular fibrosis, creatinineamia, renal interstitial fibrosis as well as the increase in fractional water excretion was prevented. <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content>\u2010induced increase in systolic blood pressure was mitigated. By contrast, endothelial dysfunction, induction of vascular inflammatory marker <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and albuminuria were not inhibited. Cardiac and cardiomyocyte hypertrophy were also not prevented by <jats:styled-content style=\"fixed-case\">VSMC<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">KO<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Vascular smooth muscle cell\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content>s are relevant for pathological <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content> action in\u00a0vivo. Our data show in\u00a0vivo and ex\u00a0vivo the necessity of <jats:styled-content style=\"fixed-case\">VSMC<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> for <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content>\u2010induced structural and functional vascular remodelling, not including endothelial dysfunction. Hereby, <jats:styled-content style=\"fixed-case\">VSMC<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">EGFR<\/jats:styled-content> gains importance for complete <jats:styled-content style=\"fixed-case\">AII<\/jats:styled-content>\u2010induced renal end\u2010organ damage succeeding vascular remodelling.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12996","type":"journal-article","created":{"date-parts":[[2017,11,20]],"date-time":"2017-11-20T05:14:39Z","timestamp":1511154879000},"source":"Crossref","is-referenced-by-count":32,"title":["Deletion of the <scp>EGF<\/scp> receptor in vascular smooth muscle cells prevents chronic angiotensin <scp>II<\/scp>\u2010induced arterial wall stiffening and media thickening"],"prefix":"10.1111","volume":"222","author":[{"given":"B.","family":"Schreier","sequence":"first","affiliation":[{"name":"Julius\u2010Bernstein\u2010Institute of Physiology Martin Luther University Halle\u2010Wittenberg Halle 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