FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3194665594> ?p ?o ?g. }

• W3194665594 endingPage "155657" @default.
• W3194665594 startingPage "155657" @default.
• W3194665594 abstract "Psoriasis is a common chronic inflammatory skin disorder that causes patches of thick red skin and silvery scales and affects 1-3% of the population, which reduces patient's quality of life. Understanding the pathogenesis of psoriasis is crucial for developing novel therapeutic strategies.HaCaT and NHEK cells were treated with TNF-α in vitro. A mouse model of psoriasis was established by topical imiquimod application on back skin. LncRNA MEG3 was cloned into the pcDNA3.1 vector and transfected in TNF-α-treated HaCaT and NHEK cells to overexpress its expression. Liposome-encapsulated pcDNA3.1-MEG3 was injected into imiquimod-treated mice via tail vein. RT-qPCR and western blot assays were used to examine the expression of lncRNA MEG3, IL-6, IL-8, IFN-γ, IL-1β, LC3, Beclin 1, p62, p-p65, p65, NLRP3, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, mTOR respectively. The secretion of IL-6, IL-8, IFN-γ and IL-1β was determined using ELISA assay. Immunofluorescence and immunohistochemistry methods were performed for analyzing the expression of LC3 and NLRP3 in cells and skin tissues respectively. LY294002 was used to block the PI3K/AKT/mTOR signalling. MTT assay was applied to test the toxicity of LY294002 to HaCaT and NHEK cells.LncRNA MEG3 expression levels were downregulated in TNF-α-treated HaCaT and NHEK cells and skin tissues of psoriatic mice model. TNF-α treatment enhanced inflammation and suppressed autophagy in HaCaT and NHEK cells, which were largely reversed by overexpression of lncRNA MEG3. Autophagy puncta and NLRP3 inflammasome assembly showed the same patterns with the expression of inflammation and autophagy markers in TNF-α-treated HaCaT and NHEK cells with or without lncRNA MEG3 overexpression. TNF-α-induced activation of the PI3K/AKT/mTOR signalling was abolished by lncRNA MEG3 overexpression in HaCaT and NHEK cells. Blocking the PI3K/AKT/mTOR signalling inhibited TNF-α-induced inflammation and restored autophagy level in TNF-α-treated HaCaT and NHEK cells. Overexpression of lncRNA MEG3 suppressed inflammation, promoted autophagy and inhibited the activation of the PI3K/AKT/mTOR signalling in a mouse model of psoriasis.LncRNA MEG3 facilitates autophagy and suppresses inflammation in TNF-α-treated keratinocytes and psoriatic mice, which is dependent on the PI3K/AKT/mTOR signalling pathway. Our study enhances the understanding of psoriasis and provides potential therapeutic targets for psoriasis." @default.
• W3194665594 created "2021-08-30" @default.
• W3194665594 creator A5003850660 @default.
• W3194665594 creator A5033739869 @default.
• W3194665594 creator A5035953140 @default.
• W3194665594 creator A5043493060 @default.
• W3194665594 creator A5055997226 @default.
• W3194665594 creator A5062137446 @default.
• W3194665594 date "2021-12-01" @default.
• W3194665594 modified "2023-10-11" @default.
• W3194665594 title "LncRNA MEG3 suppresses PI3K/AKT/mTOR signalling pathway to enhance autophagy and inhibit inflammation in TNF-α-treated keratinocytes and psoriatic mice" @default.
• W3194665594 cites W1964552652 @default.
• W3194665594 cites W1989176279 @default.
• W3194665594 cites W1991114401 @default.
• W3194665594 cites W2028536701 @default.
• W3194665594 cites W2042289037 @default.
• W3194665594 cites W2071466153 @default.
• W3194665594 cites W2109034822 @default.
• W3194665594 cites W2129375421 @default.
• W3194665594 cites W2147637490 @default.
• W3194665594 cites W2259090596 @default.
• W3194665594 cites W2324467793 @default.
• W3194665594 cites W2411755294 @default.
• W3194665594 cites W2545636599 @default.
• W3194665594 cites W2561759163 @default.
• W3194665594 cites W2596302024 @default.
• W3194665594 cites W2738580736 @default.
• W3194665594 cites W2763041471 @default.
• W3194665594 cites W2766017920 @default.
• W3194665594 cites W2769045700 @default.
• W3194665594 cites W2792707388 @default.
• W3194665594 cites W2891761389 @default.
• W3194665594 cites W2902241316 @default.
• W3194665594 cites W2924895007 @default.
• W3194665594 cites W2943588752 @default.
• W3194665594 cites W2953811896 @default.
• W3194665594 cites W2962697121 @default.
• W3194665594 cites W2967278186 @default.
• W3194665594 cites W2970225389 @default.
• W3194665594 cites W2974234421 @default.
• W3194665594 cites W2982491728 @default.
• W3194665594 cites W3004361151 @default.
• W3194665594 cites W3028355101 @default.
• W3194665594 cites W4249483860 @default.
• W3194665594 cites W4294214970 @default.
• W3194665594 doi "https://doi.org/10.1016/j.cyto.2021.155657" @default.
• W3194665594 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34425525" @default.
• W3194665594 hasPublicationYear "2021" @default.
• W3194665594 type Work @default.
• W3194665594 sameAs 3194665594 @default.
• W3194665594 citedByCount "38" @default.
• W3194665594 countsByYear W31946655942021 @default.
• W3194665594 countsByYear W31946655942022 @default.
• W3194665594 countsByYear W31946655942023 @default.
• W3194665594 crossrefType "journal-article" @default.
• W3194665594 hasAuthorship W3194665594A5003850660 @default.
• W3194665594 hasAuthorship W3194665594A5033739869 @default.
• W3194665594 hasAuthorship W3194665594A5035953140 @default.
• W3194665594 hasAuthorship W3194665594A5043493060 @default.
• W3194665594 hasAuthorship W3194665594A5055997226 @default.
• W3194665594 hasAuthorship W3194665594A5062137446 @default.
• W3194665594 hasConcept C118995209 @default.
• W3194665594 hasConcept C153911025 @default.
• W3194665594 hasConcept C185592680 @default.
• W3194665594 hasConcept C190283241 @default.
• W3194665594 hasConcept C202751555 @default.
• W3194665594 hasConcept C203014093 @default.
• W3194665594 hasConcept C203522944 @default.
• W3194665594 hasConcept C2779112978 @default.
• W3194665594 hasConcept C2780564577 @default.
• W3194665594 hasConcept C502942594 @default.
• W3194665594 hasConcept C55493867 @default.
• W3194665594 hasConcept C62478195 @default.
• W3194665594 hasConcept C75217442 @default.
• W3194665594 hasConcept C86554907 @default.
• W3194665594 hasConcept C86803240 @default.
• W3194665594 hasConcept C95444343 @default.
• W3194665594 hasConceptScore W3194665594C118995209 @default.
• W3194665594 hasConceptScore W3194665594C153911025 @default.
• W3194665594 hasConceptScore W3194665594C185592680 @default.
• W3194665594 hasConceptScore W3194665594C190283241 @default.
• W3194665594 hasConceptScore W3194665594C202751555 @default.
• W3194665594 hasConceptScore W3194665594C203014093 @default.
• W3194665594 hasConceptScore W3194665594C203522944 @default.
• W3194665594 hasConceptScore W3194665594C2779112978 @default.
• W3194665594 hasConceptScore W3194665594C2780564577 @default.
• W3194665594 hasConceptScore W3194665594C502942594 @default.
• W3194665594 hasConceptScore W3194665594C55493867 @default.
• W3194665594 hasConceptScore W3194665594C62478195 @default.
• W3194665594 hasConceptScore W3194665594C75217442 @default.
• W3194665594 hasConceptScore W3194665594C86554907 @default.
• W3194665594 hasConceptScore W3194665594C86803240 @default.
• W3194665594 hasConceptScore W3194665594C95444343 @default.
• W3194665594 hasLocation W31946655941 @default.
• W3194665594 hasLocation W31946655942 @default.
• W3194665594 hasOpenAccess W3194665594 @default.
• W3194665594 hasPrimaryLocation W31946655941 @default.
• W3194665594 hasRelatedWork W1585268103 @default.

• next