Gutenberg Open Science: Elevated intraocular pressure induces neuron-specific β-III-tubulin expression in non-neuronal vascular cells

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7094

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DC Field	Value	Language
dc.contributor.author	Prokosch, Verena	-
dc.contributor.author	Brockhaus, Kathrin	-
dc.contributor.author	Anders, Fabian	-
dc.contributor.author	Liu, Hanhan	-
dc.contributor.author	Mercieca, Karl	-
dc.contributor.author	Gericke, Adrian	-
dc.contributor.author	Melkonyan, Harut	-
dc.contributor.author	Thanos, Solon	-
dc.date.accessioned	2022-06-08T09:35:43Z	-
dc.date.available	2022-06-08T09:35:43Z	-
dc.date.issued	2020	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/7108	-
dc.description.abstract	PURPOSE Pathological alterations within optic nerve axons and progressive loss of the parental retinal ganglion cell (RGC) bodies are characteristics of glaucomatous neuropathy. Abnormally elevated intraocular pressure (IOP) is thought to be the major risk factor for most forms of glaucomatous changes, while lowering of the IOP 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 IOP harms the neurons directly or indirectly through alterations in the retinal vascularization. METHODS We analysed morphological and molecular changes within the retina exposed to elevated IOP in an animal model of glaucoma in vivo, in retinal explants and in cultured dissociated retinal cells each incubated under elevated air pressure in vitro, imitating elevated IOP. RESULTS Although ß-III-tubulin expressing RGCs decreased within the course of the disease, total amount of ß-III-tubulin protein within the retina increased, leading to the assumption that other cells than RGCs abnormally express ß-III-tubulin due to elevated IOP. Surprisingly, we found that β-III-tubulin, a marker developmentally regulated and specifically expressed in neurons under normal conditions, was strongly up-regulated in desmin-, PDGFR-β- and α-SMA-positive pericytes as well as in endothelin-1-positive endothelial cells both in vivo under elevated IOP and in vitro under elevated culture atmosphere pressure that simulated IOP elevation. Beta-III-tubulin-driven signalling pathways (ERK 1/2, pERK1/2 and cdc42/Rac) were also regulated. CONCLUSION The unprecedented regulation of neuron-specific β-III-tubulin in pericytes and endothelial cells is likely associated with a role of the retinal vasculature in the IOP-induced development and manifestation of glaucomatous degenerative optic nerve response.	en_GB
dc.language.iso	eng	de
dc.rights	CC BY-NC	*
dc.rights.uri	https://creativecommons.org/licenses/by-nc/4.0/	*
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	Elevated intraocular pressure induces neuron-specific β-III-tubulin expression in non-neuronal vascular cells	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-7094	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 04 Medizin	de
jgu.organisation.number	2700	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	Acta ophthalmologica	de
jgu.journal.volume	98	de
jgu.journal.issue	5	de
jgu.pages.start	e617	de
jgu.pages.end	e630	de
jgu.publisher.year	2020	-
jgu.publisher.name	Blackwell	de
jgu.publisher.place	Oxford	de
jgu.publisher.issn	1755-3768	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	610	de
jgu.publisher.doi	10.1111/aos.14333	de
jgu.organisation.ror	https://ror.org/023b0x485
Appears in collections:	JGU-Publikationen

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