<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Saadane A</submitter><funding>NEI NIH HHS</funding><funding>Research to Prevent Blindness</funding><funding>F. M. Kirby Foundation</funding><funding>National Institutes of Health</funding><pagination>2368-2382</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6277162</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>59(12)</volume><pubmed_abstract>Apolipoprotein E (APOE) is a component of lipid-transporting particles and a recognition ligand for receptors, which bind these particles. The APOE isoform ε2 is a risk factor for age-related macular degeneration; nevertheless, APOE absence in humans and mice does not significantly affect the retina. We found that retinal cholesterol biosynthesis and the levels of retinal cholesterol were increased in &lt;i>Apoe&lt;sup>-/-&lt;/sup>&lt;/i> mice, whereas cholesterol elimination by metabolism was decreased. No focal cholesterol deposits were observed in the &lt;i>Apoe&lt;sup>-/-&lt;/sup>&lt;/i> retina. Retinal proteomics identified the most abundant cholesterol-related proteins in WT mice and revealed that, of these cholesterol-related proteins, only APOA4 had increased expression in the &lt;i>Apoe&lt;sup>-/-&lt;/sup>&lt;/i> re</pubmed_abstract><journal>Journal of lipid research</journal><pubmed_title>Mechanisms that minimize retinal impact of apolipoprotein E absence.</pubmed_title><pmcid>PMC6277162</pmcid><funding_grant_id>P30 EY001583</funding_grant_id><funding_grant_id>EY015240</funding_grant_id><funding_grant_id>EY018383,</funding_grant_id><funding_grant_id>EY11373,</funding_grant_id><funding_grant_id>P30 EY011373</funding_grant_id><funding_grant_id>R01 EY018383</funding_grant_id><funding_grant_id>R01 EY015240</funding_grant_id><pubmed_authors>El-Darzi N</pubmed_authors><pubmed_authors>Pikuleva IA</pubmed_authors><pubmed_authors>Mast N</pubmed_authors><pubmed_authors>Saadane A</pubmed_authors><pubmed_authors>Alnemri A</pubmed_authors><pubmed_authors>Petrov A</pubmed_authors><pubmed_authors>Dao T</pubmed_authors><pubmed_authors>Dunaief JL</pubmed_authors><pubmed_authors>Song Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mechanisms that minimize retinal impact of apolipoprotein E absence.</name><description>Apolipoprotein E (APOE) is a component of lipid-transporting particles and a recognition ligand for receptors, which bind these particles. The APOE isoform ε2 is a risk factor for age-related macular degeneration; nevertheless, APOE absence in humans and mice does not significantly affect the retina. We found that retinal cholesterol biosynthesis and the levels of retinal cholesterol were increased in &lt;i>Apoe&lt;sup>-/-&lt;/sup>&lt;/i> mice, whereas cholesterol elimination by metabolism was decreased. No focal cholesterol deposits were observed in the &lt;i>Apoe&lt;sup>-/-&lt;/sup>&lt;/i> retina. Retinal proteomics identified the most abundant cholesterol-related proteins in WT mice and revealed that, of these cholesterol-related proteins, only APOA4 had increased expression in the &lt;i>Apoe&lt;sup>-/-&lt;/sup>&lt;/i> re</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Dec</publication><modification>2025-04-07T12:28:51.179Z</modification><creation>2025-04-07T12:28:51.179Z</creation></dates><accession>S-EPMC6277162</accession><cross_references><pubmed>30333155</pubmed><doi>10.1194/jlr.M090043</doi><doi>10.1194/jlr.m090043</doi></cross_references></HashMap>