<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Perumal N</submitter><funding>Deutsche Forschungsgemeinschaft</funding><pagination>101597</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7327981</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>34</volume><pubmed_abstract>Ocular vascular dysfunction is a major contributing factor to the pathogenesis of glaucoma. In recent years, there has been a renewed interest in the role of angiotensin II (Ang II) in mediating the disease progression. Despite its (patho)physiological importance, the molecular mechanisms underlying Ang II-mediated oxidative stress remain largely unexplored in the ocular vasculature. Here, we provide the first direct evidence of the alterations of proteome and signalling pathways underlying Ang II-elicited oxidative insult independent of arterial pressure changes in the ophthalmic artery (OA) and retina (R) employing an in vitro experimental model. Both R and OA were isolated from male C57Bl/6J mice (n = 15/group; n = 5/biological replicate) and incubated overnight in medium containing eit</pubmed_abstract><journal>Redox biology</journal><pubmed_title>Bioenergetic shift and actin cytoskeleton remodelling as acute vascular adaptive mechanisms to angiotensin II in murine retina and ophthalmic artery.</pubmed_title><pmcid>PMC7327981</pmcid><funding_grant_id>MA 8006/1-1</funding_grant_id><pubmed_authors>Straßburger L</pubmed_authors><pubmed_authors>Grus FH</pubmed_authors><pubmed_authors>Manicam C</pubmed_authors><pubmed_authors>Pfeiffer N</pubmed_authors><pubmed_authors>Herzog DP</pubmed_authors><pubmed_authors>Perumal N</pubmed_authors><pubmed_authors>Muller MB</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bioenergetic shift and actin cytoskeleton remodelling as acute vascular adaptive mechanisms to angiotensin II in murine retina and ophthalmic artery.</name><description>Ocular vascular dysfunction is a major contributing factor to the pathogenesis of glaucoma. In recent years, there has been a renewed interest in the role of angiotensin II (Ang II) in mediating the disease progression. Despite its (patho)physiological importance, the molecular mechanisms underlying Ang II-mediated oxidative stress remain largely unexplored in the ocular vasculature. Here, we provide the first direct evidence of the alterations of proteome and signalling pathways underlying Ang II-elicited oxidative insult independent of arterial pressure changes in the ophthalmic artery (OA) and retina (R) employing an in vitro experimental model. Both R and OA were isolated from male C57Bl/6J mice (n = 15/group; n = 5/biological replicate) and incubated overnight in medium containing eit</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jul</publication><modification>2026-05-09T00:33:14.354Z</modification><creation>2020-07-10T07:18:59Z</creation></dates><accession>S-EPMC7327981</accession><cross_references><pubmed>32513477</pubmed><doi>10.1016/j.redox.2020.101597</doi></cross_references></HashMap>