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Abnormally elevated intraocular pressure (<jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content>) is thought to be the major risk factor for most forms of glaucomatous changes, while lowering of the <jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content> is the mainstream of treatment. However, the pathophysiological mechanisms involved in neurodegenerative changes are poorly understood. It remains still a matter of debate whether elevated <jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content> harms the neurons directly or indirectly through alterations in the retinal vascularization.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We analysed morphological and molecular changes within the retina exposed to elevated <jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content> in an animal model of glaucoma <jats:italic>in vivo<\/jats:italic>, in retinal explants and in cultured dissociated retinal cells each incubated under elevated air pressure <jats:italic>in vitro<\/jats:italic>, imitating elevated IOP.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Although \u00df\u2010<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>\u2010tubulin expressing <jats:styled-content style=\"fixed-case\">RGC<\/jats:styled-content>s decreased within the course of the disease, total amount of \u00df\u2010<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>\u2010tubulin protein within the retina increased, leading to the assumption that other cells than <jats:styled-content style=\"fixed-case\">RGC<\/jats:styled-content>s abnormally express \u00df\u2010<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>\u2010tubulin due to elevated <jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content>. Surprisingly, we found that \u03b2\u2010<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>\u2010tubulin, a marker developmentally regulated and specifically expressed in neurons under normal conditions, was strongly up\u2010regulated in desmin\u2010, <jats:styled-content style=\"fixed-case\">PDGFR<\/jats:styled-content>\u2010\u03b2\u2010 and \u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>\u2010positive pericytes as well as in endothelin\u20101\u2010positive endothelial cells both <jats:italic>in vivo<\/jats:italic> under elevated <jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content> and <jats:italic>in vitro<\/jats:italic> under elevated culture atmosphere pressure that simulated <jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content> elevation. Beta\u2010<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>\u2010tubulin\u2010driven signalling pathways (<jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content> 1\/2, <jats:styled-content style=\"fixed-case\">pERK<\/jats:styled-content>1\/2 and cdc42\/Rac) were also regulated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The unprecedented regulation of neuron\u2010specific \u03b2\u2010<jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>\u2010tubulin in pericytes and endothelial cells is likely associated with a role of the retinal vasculature in the <jats:styled-content style=\"fixed-case\">IOP<\/jats:styled-content>\u2010induced development and manifestation of glaucomatous degenerative optic nerve response.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aos.14333","type":"journal-article","created":{"date-parts":[[2019,12,30]],"date-time":"2019-12-30T06:34:45Z","timestamp":1577687685000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Elevated intraocular pressure induces neuron\u2010specific \u03b2\u2010<scp>III<\/scp>\u2010tubulin expression in non\u2010neuronal vascular cells"],"prefix":"10.1111","volume":"98","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5318-0637","authenticated-orcid":false,"given":"Verena","family":"Prokosch","sequence":"first","affiliation":[{"name":"Institute of Experimental Ophthalmology and DFG\u2010Center of Excellence Cells in Motion (CIM) School of Medicine Westfalian\u2010Wilhelms\u2010University of M\u00fcnster Munster Germany"},{"name":"University Eye Hospital Mainz Johannes Gutenberg University of Mainz Mainz 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