FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3128293887> ?p ?o ?g. }

• W3128293887 abstract "Abstract Background Abnormal neovascularization is the most common cause of blindness, and hypoxia alters tissue metabolism, function, and morphology. HIF-1α, the transcriptional activator of VEGF, has intricate mechanisms of nuclear translocation and activation, but its signal termination mechanisms remain unclear. Methods We investigated the role of polypyrimidine tract-binding protein-associated splicing factor (PSF) in cellular energy production, migration, and proliferation by targeting HIF-1α in vivo and in vitro PSF plasmids were transfected with liposome 2000 transfection reagent. Young C57/BL6J mice were kept in a hyperoxia environment, followed by indoor air, resulting in oxygen-induced retinopathy. Oxygen-induced retinopathy (OIR) animals were randomly divided into three groups: OIR group, OIR + vector group (OIR cubs treated with rAAV vector) and OIR + PSF group (OIR cubs treated with rAAV-PSF). Age-matched C57/BL6J mice were used as controls and exposed to constant normoxic conditions. The animals were executed and their pupils were subjected to subsequent experiments. The metabolic spectrum was analyzed by Seahorse XFe96 flux analyzer, and OCR and extracellular acidification rate were quantified at the same time. Results PSF ameliorated retinal neovascularization and corrected abnormal VEGF expression in mice with oxygen-induced retinopathy and reduced intra-retinal neovascularization in Vldlr − / − mice. PSF reprogrammed mitochondrial bioenergetics and inhibited the transition of endothelial cells after hypoxia, suggesting its involvement in pathological angiogenesis.Ectopic PSF expression inhibited hypoxia-induced HIF-1α activation in the nucleus by recruiting Hakai to the PSF/HIF-1α complex, causing HIF-1α inhibition. PSF knockdown increased hypoxia-stimulated HIF-1α reactions. These hypoxia-dependent processes may play a vital role in cell metabolism, migration, and proliferation. Thus, PSF is a potential treatment target in neovascularization-associated ophthalmopathy. Conclusion This is the first study showing that PSF inhibits HIF-1α via recruitment of Hakai, modulates mitochondrial oxidation and glycolysis, and downregulates VEGF expression under hypoxia. We propose a new HIF-1 α/Hakai regulatory mechanism that may play a vital role in the pathogenesis of neovascularization in ophthalmopathy. PSF-Hakai–HIF-1α signaling pathway under hypoxia condition. Schematic diagram showing that the PSF-Hakai–HIF-1α signaling pathway. Under hypoxia condition, PSF-Hakai complex regulate HIF-1α signaling, thus inhibiting downstream target gene VEGF, cell metabolism and angiogenesis eventually." @default.
• W3128293887 created "2021-02-15" @default.
• W3128293887 creator A5006034039 @default.
• W3128293887 creator A5011687047 @default.
• W3128293887 creator A5012486505 @default.
• W3128293887 creator A5043852609 @default.
• W3128293887 creator A5056640120 @default.
• W3128293887 creator A5073593485 @default.
• W3128293887 creator A5085181392 @default.
• W3128293887 date "2021-02-11" @default.
• W3128293887 modified "2023-09-24" @default.
• W3128293887 title "PSF functions as a repressor of hypoxia-induced angiogenesis by promoting mitochondrial function" @default.
• W3128293887 cites W1744742580 @default.
• W3128293887 cites W1967945239 @default.
• W3128293887 cites W1994344724 @default.
• W3128293887 cites W1999828349 @default.
• W3128293887 cites W1999847819 @default.
• W3128293887 cites W2009516966 @default.
• W3128293887 cites W2015887548 @default.
• W3128293887 cites W2018468829 @default.
• W3128293887 cites W2022473598 @default.
• W3128293887 cites W2031171659 @default.
• W3128293887 cites W2046298589 @default.
• W3128293887 cites W2050819567 @default.
• W3128293887 cites W2064007275 @default.
• W3128293887 cites W2078234461 @default.
• W3128293887 cites W2091597591 @default.
• W3128293887 cites W2144625075 @default.
• W3128293887 cites W2167537448 @default.
• W3128293887 cites W2591395115 @default.
• W3128293887 cites W2682666440 @default.
• W3128293887 cites W2790130572 @default.
• W3128293887 cites W2804718180 @default.
• W3128293887 cites W2806918958 @default.
• W3128293887 cites W2828456915 @default.
• W3128293887 cites W2905607079 @default.
• W3128293887 cites W2909906311 @default.
• W3128293887 cites W2918845011 @default.
• W3128293887 cites W2920344014 @default.
• W3128293887 cites W2949312182 @default.
• W3128293887 cites W2951640072 @default.
• W3128293887 cites W2955894052 @default.
• W3128293887 cites W2970385120 @default.
• W3128293887 cites W2978828567 @default.
• W3128293887 cites W2982366104 @default.
• W3128293887 cites W2997153159 @default.
• W3128293887 cites W3029713241 @default.
• W3128293887 doi "https://doi.org/10.1186/s12964-020-00684-w" @default.
• W3128293887 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7879653" @default.
• W3128293887 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33573690" @default.
• W3128293887 hasPublicationYear "2021" @default.
• W3128293887 type Work @default.
• W3128293887 sameAs 3128293887 @default.
• W3128293887 citedByCount "10" @default.
• W3128293887 countsByYear W31282938872021 @default.
• W3128293887 countsByYear W31282938872022 @default.
• W3128293887 countsByYear W31282938872023 @default.
• W3128293887 crossrefType "journal-article" @default.
• W3128293887 hasAuthorship W3128293887A5006034039 @default.
• W3128293887 hasAuthorship W3128293887A5011687047 @default.
• W3128293887 hasAuthorship W3128293887A5012486505 @default.
• W3128293887 hasAuthorship W3128293887A5043852609 @default.
• W3128293887 hasAuthorship W3128293887A5056640120 @default.
• W3128293887 hasAuthorship W3128293887A5073593485 @default.
• W3128293887 hasAuthorship W3128293887A5085181392 @default.
• W3128293887 hasBestOaLocation W31282938871 @default.
• W3128293887 hasConcept C153911025 @default.
• W3128293887 hasConcept C178790620 @default.
• W3128293887 hasConcept C185592680 @default.
• W3128293887 hasConcept C2778271429 @default.
• W3128293887 hasConcept C2780394083 @default.
• W3128293887 hasConcept C2780827179 @default.
• W3128293887 hasConcept C502942594 @default.
• W3128293887 hasConcept C540031477 @default.
• W3128293887 hasConcept C54009773 @default.
• W3128293887 hasConcept C54355233 @default.
• W3128293887 hasConcept C55493867 @default.
• W3128293887 hasConcept C7836513 @default.
• W3128293887 hasConcept C81885089 @default.
• W3128293887 hasConcept C86803240 @default.
• W3128293887 hasConcept C95444343 @default.
• W3128293887 hasConceptScore W3128293887C153911025 @default.
• W3128293887 hasConceptScore W3128293887C178790620 @default.
• W3128293887 hasConceptScore W3128293887C185592680 @default.
• W3128293887 hasConceptScore W3128293887C2778271429 @default.
• W3128293887 hasConceptScore W3128293887C2780394083 @default.
• W3128293887 hasConceptScore W3128293887C2780827179 @default.
• W3128293887 hasConceptScore W3128293887C502942594 @default.
• W3128293887 hasConceptScore W3128293887C540031477 @default.
• W3128293887 hasConceptScore W3128293887C54009773 @default.
• W3128293887 hasConceptScore W3128293887C54355233 @default.
• W3128293887 hasConceptScore W3128293887C55493867 @default.
• W3128293887 hasConceptScore W3128293887C7836513 @default.
• W3128293887 hasConceptScore W3128293887C81885089 @default.
• W3128293887 hasConceptScore W3128293887C86803240 @default.
• W3128293887 hasConceptScore W3128293887C95444343 @default.
• W3128293887 hasFunder F4320321001 @default.
• W3128293887 hasIssue "1" @default.
• W3128293887 hasLocation W31282938871 @default.
• W3128293887 hasLocation W31282938872 @default.

• next