FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2333485780> ?p ?o ?g. }

• W2333485780 endingPage "531" @default.
• W2333485780 startingPage "531" @default.
• W2333485780 abstract "Abstract Introduction Cardiac hypertrophy is an adaptive response of the heart to prolonged increases in hemodynamic workload. This compensatory process is initially beneficial in normalizing wall stress, and sustained left ventricular hypertrophy significantly increases the risk of developing heart failure. Although various molecules have been shown to be involved in the compensatory process, its molecular mechanism still remains unclear. We investigated roles of IFN-γ in the process of compensatory cardiac hypertrophy induced by pressure overload. Methods Male Balb/c (WT) and IFN-γ-deficient (IFN-γ-KO) mice were subjected to transverse aortic constriction (TAC).Aortic constriction was achieved by tying around the transverse thoracic aorta against a 28-gauge needle using a 7–0 silk suture, and then removing the needle. As the control, sham operation was also performed without constricting the aorta. Cardiac hypertrophy, survival rate and hypertrophy related signaling pathways were examined. Results Intracardiac gene expression for IFN-γ was rapidly increased in TAC mice. Although TAC induced rapid increase of heart weight/body weight ratio (HW/BW ratio) in WT mice even at 3 days after TAC, most mice survived for 3 weeks after TAC. On the other hand, IFN-γ-KO mice showed no significant increase of HW/BW ratio at 3 days after TAC, and about 60% of them died within 6 days after TAC. Western blotting analysis showed that AKT phosphorylation in the left ventricles of WT mice was significantly increased at 3 days after TAC, compared with sham operated mice. The downstream signal molecules, GSK-3 β and GATA4, were also highly phosphorylated in the left ventricles of WT mice, compared with sham operated mice. However, the activation of PI3K/AKT signals were significantly attenuated in the left ventricles of IFN-γ-KO mice, indicating that IFN-γ plays a crucial role in the hypertrophic response through PI3K/AKT signaling. Conclusion Our results demonstrate blunted hypertrophy with reduced survival rate and attenuated PIK3/AKT signaling following pressure overload in IFN-γ-KO mice, and suggest that IFN-γ plays a crucial role in the compensatory hypertrophic response." @default.
• W2333485780 created "2016-06-24" @default.
• W2333485780 creator A5003684777 @default.
• W2333485780 creator A5017023363 @default.
• W2333485780 creator A5025184711 @default.
• W2333485780 creator A5045762902 @default.
• W2333485780 creator A5050194752 @default.
• W2333485780 creator A5086426648 @default.
• W2333485780 creator A5089466691 @default.
• W2333485780 date "2012-09-01" @default.
• W2333485780 modified "2023-09-26" @default.
• W2333485780 title "P038 A role of IFN-gamma in pressure overload-induced compensatory cardiac hypertrophy" @default.
• W2333485780 doi "https://doi.org/10.1016/j.cyto.2012.06.122" @default.
• W2333485780 hasPublicationYear "2012" @default.
• W2333485780 type Work @default.
• W2333485780 sameAs 2333485780 @default.
• W2333485780 citedByCount "0" @default.
• W2333485780 crossrefType "journal-article" @default.
• W2333485780 hasAuthorship W2333485780A5003684777 @default.
• W2333485780 hasAuthorship W2333485780A5017023363 @default.
• W2333485780 hasAuthorship W2333485780A5025184711 @default.
• W2333485780 hasAuthorship W2333485780A5045762902 @default.
• W2333485780 hasAuthorship W2333485780A5050194752 @default.
• W2333485780 hasAuthorship W2333485780A5086426648 @default.
• W2333485780 hasAuthorship W2333485780A5089466691 @default.
• W2333485780 hasConcept C126322002 @default.
• W2333485780 hasConcept C164705383 @default.
• W2333485780 hasConcept C167414201 @default.
• W2333485780 hasConcept C2778271984 @default.
• W2333485780 hasConcept C2910639518 @default.
• W2333485780 hasConcept C3018791406 @default.
• W2333485780 hasConcept C71924100 @default.
• W2333485780 hasConceptScore W2333485780C126322002 @default.
• W2333485780 hasConceptScore W2333485780C164705383 @default.
• W2333485780 hasConceptScore W2333485780C167414201 @default.
• W2333485780 hasConceptScore W2333485780C2778271984 @default.
• W2333485780 hasConceptScore W2333485780C2910639518 @default.
• W2333485780 hasConceptScore W2333485780C3018791406 @default.
• W2333485780 hasConceptScore W2333485780C71924100 @default.
• W2333485780 hasIssue "3" @default.
• W2333485780 hasLocation W23334857801 @default.
• W2333485780 hasOpenAccess W2333485780 @default.
• W2333485780 hasPrimaryLocation W23334857801 @default.
• W2333485780 hasRelatedWork W134355629 @default.
• W2333485780 hasRelatedWork W2028354341 @default.
• W2333485780 hasRelatedWork W2029120861 @default.
• W2333485780 hasRelatedWork W2052926718 @default.
• W2333485780 hasRelatedWork W2095147394 @default.
• W2333485780 hasRelatedWork W2125138303 @default.
• W2333485780 hasRelatedWork W2167689189 @default.
• W2333485780 hasRelatedWork W2561965823 @default.
• W2333485780 hasRelatedWork W2764849705 @default.
• W2333485780 hasRelatedWork W2800256347 @default.
• W2333485780 hasVolume "59" @default.
• W2333485780 isParatext "false" @default.
• W2333485780 isRetracted "false" @default.
• W2333485780 magId "2333485780" @default.
• W2333485780 workType "article" @default.