FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3081789279> ?p ?o ?g. }

• W3081789279 abstract "Abstract Background Glaucoma is a leading neurodegenerative disease affecting over 70 million individuals worldwide. Early pathological events of axonal degeneration and retinopathy in response to elevated intraocular pressure (IOP) are limited and not well-defined due to the lack of appropriate animal models that faithfully replicate all the phenotypes of primary open angle glaucoma (POAG), the most common form of glaucoma. Glucocorticoid (GC)-induced ocular hypertension (OHT) and its associated iatrogenic open-angle glaucoma share many features with POAG. Here, we characterized a novel mouse model of GC-induced OHT for glaucomatous neurodegeneration and further explored early pathological events of axonal degeneration in response to elevated IOP. Methods C57BL/6 J mice were periocularly injected with either vehicle or the potent GC, dexamethasone 21-acetate (Dex) once a week for 10 weeks. Glaucoma phenotypes including IOP, outflow facility, structural and functional loss of retinal ganglion cells (RGCs), optic nerve (ON) degeneration, gliosis, and anterograde axonal transport deficits were examined at various stages of OHT. Results Prolonged treatment with Dex leads to glaucoma in mice similar to POAG patients including IOP elevation due to reduced outflow facility and dysfunction of trabecular meshwork, progressive ON degeneration and structural and functional loss of RGCs. Lowering of IOP rescued Dex-induced ON degeneration and RGC loss, suggesting that glaucomatous neurodegeneration is IOP dependent. Also, Dex-induced neurodegeneration was associated with activation of astrocytes, axonal transport deficits, ON demyelination, mitochondrial accumulation and immune cell infiltration in the optic nerve head (ONH) region. Our studies further show that ON degeneration precedes structural and functional loss of RGCs in Dex-treated mice. Axonal damage and transport deficits initiate at the ONH and progress toward the distal end of ON and target regions in the brain (i.e. superior colliculus). Most of anterograde transport was preserved during initial stages of axonal degeneration (30% loss) and complete transport deficits were only observed at the ONH during later stages of severe axonal degeneration (50% loss). Conclusions These findings indicate that ON degeneration and transport deficits at the ONH precede RGC structural and functional loss and provide a new potential therapeutic window for rescuing neuronal loss and restoring health of damaged axons in glaucoma." @default.
• W3081789279 created "2020-09-08" @default.
• W3081789279 creator A5032854236 @default.
• W3081789279 creator A5047929182 @default.
• W3081789279 creator A5061662773 @default.
• W3081789279 creator A5070923637 @default.
• W3081789279 creator A5082116311 @default.
• W3081789279 creator A5089627519 @default.
• W3081789279 creator A5091517834 @default.
• W3081789279 date "2020-08-27" @default.
• W3081789279 modified "2023-10-15" @default.
• W3081789279 title "CNS axonal degeneration and transport deficits at the optic nerve head precede structural and functional loss of retinal ganglion cells in a mouse model of glaucoma" @default.
• W3081789279 cites W118598956 @default.
• W3081789279 cites W133187383 @default.
• W3081789279 cites W1504492140 @default.
• W3081789279 cites W1574402411 @default.
• W3081789279 cites W1667265675 @default.
• W3081789279 cites W1975731265 @default.
• W3081789279 cites W1978392572 @default.
• W3081789279 cites W1986862398 @default.
• W3081789279 cites W1993597268 @default.
• W3081789279 cites W1996005642 @default.
• W3081789279 cites W1996690280 @default.
• W3081789279 cites W2000182546 @default.
• W3081789279 cites W2000989960 @default.
• W3081789279 cites W2017030433 @default.
• W3081789279 cites W2019885109 @default.
• W3081789279 cites W2021586614 @default.
• W3081789279 cites W2021933371 @default.
• W3081789279 cites W2022209206 @default.
• W3081789279 cites W2023036475 @default.
• W3081789279 cites W2023691343 @default.
• W3081789279 cites W2024776123 @default.
• W3081789279 cites W2026080360 @default.
• W3081789279 cites W2049862190 @default.
• W3081789279 cites W2050232773 @default.
• W3081789279 cites W2050438215 @default.
• W3081789279 cites W2055600586 @default.
• W3081789279 cites W2057266151 @default.
• W3081789279 cites W2062457533 @default.
• W3081789279 cites W2067215143 @default.
• W3081789279 cites W2072593442 @default.
• W3081789279 cites W2078077142 @default.
• W3081789279 cites W2078684091 @default.
• W3081789279 cites W2084941189 @default.
• W3081789279 cites W2089283912 @default.
• W3081789279 cites W2091181665 @default.
• W3081789279 cites W2091823156 @default.
• W3081789279 cites W2123598898 @default.
• W3081789279 cites W2129418510 @default.
• W3081789279 cites W2130206051 @default.
• W3081789279 cites W2138974681 @default.
• W3081789279 cites W2145192598 @default.
• W3081789279 cites W2160605010 @default.
• W3081789279 cites W2163925135 @default.
• W3081789279 cites W2171679548 @default.
• W3081789279 cites W2206998273 @default.
• W3081789279 cites W2213541252 @default.
• W3081789279 cites W2287928389 @default.
• W3081789279 cites W2397854391 @default.
• W3081789279 cites W2413901835 @default.
• W3081789279 cites W2521776509 @default.
• W3081789279 cites W2580035316 @default.
• W3081789279 cites W2585778931 @default.
• W3081789279 cites W2586457419 @default.
• W3081789279 cites W2589298595 @default.
• W3081789279 cites W2607574901 @default.
• W3081789279 cites W2625521663 @default.
• W3081789279 cites W2766952000 @default.
• W3081789279 cites W2773334807 @default.
• W3081789279 cites W2790261966 @default.
• W3081789279 cites W2799291895 @default.
• W3081789279 cites W2910975531 @default.
• W3081789279 cites W2913823950 @default.
• W3081789279 cites W2921565902 @default.
• W3081789279 cites W2945985580 @default.
• W3081789279 cites W2977587116 @default.
• W3081789279 cites W4247634877 @default.
• W3081789279 cites W4255480014 @default.
• W3081789279 cites W4381931134 @default.
• W3081789279 cites W4657569 @default.
• W3081789279 cites W612404357 @default.
• W3081789279 cites W9772542 @default.
• W3081789279 doi "https://doi.org/10.1186/s13024-020-00400-9" @default.
• W3081789279 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7457267" @default.
• W3081789279 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32854767" @default.
• W3081789279 hasPublicationYear "2020" @default.
• W3081789279 type Work @default.
• W3081789279 sameAs 3081789279 @default.
• W3081789279 citedByCount "39" @default.
• W3081789279 countsByYear W30817892792020 @default.
• W3081789279 countsByYear W30817892792021 @default.
• W3081789279 countsByYear W30817892792022 @default.
• W3081789279 countsByYear W30817892792023 @default.
• W3081789279 crossrefType "journal-article" @default.
• W3081789279 hasAuthorship W3081789279A5032854236 @default.
• W3081789279 hasAuthorship W3081789279A5047929182 @default.
• W3081789279 hasAuthorship W3081789279A5061662773 @default.
• W3081789279 hasAuthorship W3081789279A5070923637 @default.
• W3081789279 hasAuthorship W3081789279A5082116311 @default.

• next