{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T00:15:33Z","timestamp":1791159333302,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,9,23]],"date-time":"2012-09-23T00:00:00Z","timestamp":1348358400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Ophthalmologica"],"published-print":{"date-parts":[[2012,11]]},"abstract":"<jats:title>Abstract.<\/jats:title><jats:p><jats:bold>Purpose:\u2002<\/jats:bold> Our previous studies suggested that CYP46A1 and 24S\u2010hydroxycholesterol (24SOH) may be associated with glaucoma. Loss of CYP46A1\u2010expressing retinal ganglion cells is involved in the activation of glia, and therefore possibly in the disbalance of cholesterol. In this context, the purpose of our present work was to emphasize the glial and longitudinal CYP46A1 expression after an interventional glaucoma\u2010related stress triggered by elevated intraocular pressure (IOP).<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> Sprague\u2013Dawley rats were submitted to laser photocoagulation of the trabecular meshwork, limbus and episcleral veins in one eye to induce elevated IOP. Rats were euthanized at days 3, 14, 30 and 60 (<jats:italic>n\u2003<\/jats:italic>=\u200310 per time\u2010point), and 24SOH was measured in plasma and retina by gas chromatography\u2013mass spectrometry. CYP46A1 was quantified by Western blotting. Glial activation was assessed by glial fibrillary acidic protein immunoreactivity in Western blots and retinal cryosections.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Sustained high IOP was observed in experimental eyes from day 1 to day 21. Plasma MCP\u20101 and ICAM\u20101, quantified using multiplex assay kits, were increased at day 3. Glial activation was observed bilaterally at all time\u2010points, at lower levels in contralateral eyes than in experimental eyes. In experimental retinas, CYP46A1 expression showed a transient increase at day 3 and then returned to baseline. Plasma and retinal 24SOH peaked at day 14 and 30, respectively.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold> These data show that CYP46A1 expression was induced early in response to retinal stress but remained constant at late time\u2010points, reinforcing the constitutive role of CYP46A1 in maintaining cholesterol balance in neuronal tissues.<\/jats:p>","DOI":"10.1111\/j.1755-3768.2012.02490.x","type":"journal-article","created":{"date-parts":[[2012,9,24]],"date-time":"2012-09-24T01:35:09Z","timestamp":1348450509000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Steady\u2010state levels of retinal 24S\u2010hydroxycholesterol are maintained by glial cells intervention after elevation of intraocular pressure in the 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