FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4220855076> ?p ?o ?g. }

• W4220855076 endingPage "645" @default.
• W4220855076 startingPage "631" @default.
• W4220855076 abstract "What is the central question of this study? What is the relationship of chemokine (C-C motif) ligand 8 (CCL8) to thoracic aortic aneurysm and dissection (TAAD) formation in postnatal mice with vascular smooth muscle cell (VSMC) Tgfbr2 disruption, and is dexamethasone a potential treatment? What is the main finding and its importance? CCL8 was associated with the formation of TAAD in VSMC Tgfbr2-disrupted mice. Dexamethasone reduced TAAD formation and inhibited mitogen-activated protein kinase (p-p38) and nuclear factor-κB (p-p65) signalling pathways. CCL8 might be an important promoter of aortic inflammation. Dexamethasone provided potential therapeutic effects in TAAD treatment.Aortic inflammation plays a vital role in initiation and progression of thoracic aortic aneurysm and dissection (TAAD). Disturbance of the transforming growth factor-β (TGF-β) signalling pathway is believed to be one of the pathogenic mechanisms of TAAD. Initially, Myh11-CreERT2 .Tgfbr2f/f male mice were used to build a TAAD mouse model, and bioinformatic analyses revealed enriched inflammatory signal pathways and upregulated chemokine (C-C motif) ligand 8 (CCL8). So we hypothesized that vascular smooth muscle cell (VSMC) Tgfbr2 disruption in postnatal mice results in aortic inflammation associated with CCL8 secretion. Real-time quantitative PCR and serum enzyme-linked immunosorbent assay (ELISA) results confirmed that CCL8 expression began to increase after VSMC Tgfbr2 disruption. Next, we cultured mouse thoracic aortas ex vivo, and observed that the protein expression of CCL8 in culture supernatants was increased by ELISA. Subsequently, the co-localization of CCL8 with α-smooth muscle actin or CD68 was found to be significantly increased by immunofluorescence. Then, dexamethasone (DEX) was used to treat TAAD in VSMC Tgfbr2-disrupted mice; the results of histochemical, immunofluorescence and immunohistochemical staining indicated that DEX therapy reduced CCL8 secretion, inflammatory cell recruitment, aortic medial thickening, elastic fibre fragmentation, extracellular matrix degradation and contractile apparatus impairment, and thereby ameliorated TAAD formation. Western blotting showed that mitogen-activated protein kinase and nuclear factor-κB signalling pathways in aorta were overactivated after VSMC Tgfbr2 disruption, but inhibited by DEX therapy. Altogether, CCL8 might be an important promoter in TAAD formation of VSMC Tgfbr2-disrupted mice, and DEX provided potential therapeutic effects in TAAD treatment." @default.
• W4220855076 created "2022-04-03" @default.
• W4220855076 creator A5000432967 @default.
• W4220855076 creator A5017676873 @default.
• W4220855076 creator A5024664435 @default.
• W4220855076 creator A5025849084 @default.
• W4220855076 creator A5028467654 @default.
• W4220855076 creator A5035701638 @default.
• W4220855076 creator A5044083204 @default.
• W4220855076 creator A5075248303 @default.
• W4220855076 creator A5081564284 @default.
• W4220855076 creator A5087912603 @default.
• W4220855076 date "2022-05-26" @default.
• W4220855076 modified "2023-10-17" @default.
• W4220855076 title "Dexamethasone attenuated thoracic aortic aneurysm and dissection in vascular smooth muscle cell <i>Tgfbr2</i> disrupted mice with CCL8 suppression" @default.
• W4220855076 cites W1490920363 @default.
• W4220855076 cites W1991791672 @default.
• W4220855076 cites W2016769140 @default.
• W4220855076 cites W2028116663 @default.
• W4220855076 cites W2053715750 @default.
• W4220855076 cites W2083104211 @default.
• W4220855076 cites W2114232003 @default.
• W4220855076 cites W2114249763 @default.
• W4220855076 cites W2122588714 @default.
• W4220855076 cites W2155248983 @default.
• W4220855076 cites W2158094210 @default.
• W4220855076 cites W2253818064 @default.
• W4220855076 cites W2569369624 @default.
• W4220855076 cites W2766610038 @default.
• W4220855076 cites W2771773353 @default.
• W4220855076 cites W2893771199 @default.
• W4220855076 cites W2911525027 @default.
• W4220855076 cites W2921353286 @default.
• W4220855076 cites W2979865036 @default.
• W4220855076 cites W2997911677 @default.
• W4220855076 cites W3019008651 @default.
• W4220855076 cites W3027722222 @default.
• W4220855076 cites W3123379912 @default.
• W4220855076 cites W3166071489 @default.
• W4220855076 doi "https://doi.org/10.1113/ep090190" @default.
• W4220855076 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35344629" @default.
• W4220855076 hasPublicationYear "2022" @default.
• W4220855076 type Work @default.
• W4220855076 citedByCount "0" @default.
• W4220855076 crossrefType "journal-article" @default.
• W4220855076 hasAuthorship W4220855076A5000432967 @default.
• W4220855076 hasAuthorship W4220855076A5017676873 @default.
• W4220855076 hasAuthorship W4220855076A5024664435 @default.
• W4220855076 hasAuthorship W4220855076A5025849084 @default.
• W4220855076 hasAuthorship W4220855076A5028467654 @default.
• W4220855076 hasAuthorship W4220855076A5035701638 @default.
• W4220855076 hasAuthorship W4220855076A5044083204 @default.
• W4220855076 hasAuthorship W4220855076A5075248303 @default.
• W4220855076 hasAuthorship W4220855076A5081564284 @default.
• W4220855076 hasAuthorship W4220855076A5087912603 @default.
• W4220855076 hasConcept C104317684 @default.
• W4220855076 hasConcept C126322002 @default.
• W4220855076 hasConcept C127561419 @default.
• W4220855076 hasConcept C13373296 @default.
• W4220855076 hasConcept C134018914 @default.
• W4220855076 hasConcept C164027704 @default.
• W4220855076 hasConcept C185592680 @default.
• W4220855076 hasConcept C203014093 @default.
• W4220855076 hasConcept C2776914184 @default.
• W4220855076 hasConcept C2777323849 @default.
• W4220855076 hasConcept C2779395532 @default.
• W4220855076 hasConcept C2779980429 @default.
• W4220855076 hasConcept C2780847584 @default.
• W4220855076 hasConcept C2992686903 @default.
• W4220855076 hasConcept C502942594 @default.
• W4220855076 hasConcept C55493867 @default.
• W4220855076 hasConcept C71924100 @default.
• W4220855076 hasConcept C86803240 @default.
• W4220855076 hasConcept C95444343 @default.
• W4220855076 hasConceptScore W4220855076C104317684 @default.
• W4220855076 hasConceptScore W4220855076C126322002 @default.
• W4220855076 hasConceptScore W4220855076C127561419 @default.
• W4220855076 hasConceptScore W4220855076C13373296 @default.
• W4220855076 hasConceptScore W4220855076C134018914 @default.
• W4220855076 hasConceptScore W4220855076C164027704 @default.
• W4220855076 hasConceptScore W4220855076C185592680 @default.
• W4220855076 hasConceptScore W4220855076C203014093 @default.
• W4220855076 hasConceptScore W4220855076C2776914184 @default.
• W4220855076 hasConceptScore W4220855076C2777323849 @default.
• W4220855076 hasConceptScore W4220855076C2779395532 @default.
• W4220855076 hasConceptScore W4220855076C2779980429 @default.
• W4220855076 hasConceptScore W4220855076C2780847584 @default.
• W4220855076 hasConceptScore W4220855076C2992686903 @default.
• W4220855076 hasConceptScore W4220855076C502942594 @default.
• W4220855076 hasConceptScore W4220855076C55493867 @default.
• W4220855076 hasConceptScore W4220855076C71924100 @default.
• W4220855076 hasConceptScore W4220855076C86803240 @default.
• W4220855076 hasConceptScore W4220855076C95444343 @default.
• W4220855076 hasFunder F4320321001 @default.
• W4220855076 hasFunder F4320322919 @default.
• W4220855076 hasIssue "6" @default.
• W4220855076 hasLocation W42208550761 @default.
• W4220855076 hasLocation W42208550762 @default.

• next