FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2981736579> ?p ?o ?g. }

• W2981736579 abstract "Abstract Background Circulating microRNAs (miRNAs) are actively transported, via inclusion in extracellular microvesicles/exosomes (herein named cardiosomes since they are deriving from cardiomyocytes), allowing protection from degradation and underlying cell-cell communications. After myocardial infarction (MI), quiescent cardiac fibroblasts can acquire an activated phenotype, and a recognized marker of such activation is the expression of α-smooth muscle actin (α-SMA); such cells are commonly known as myofibroblasts. Hypothesis We hypothesize that cardiosomal miRNAs play a pivotal role in the activation of myofibroblasts following ischemic injury. Methods Using an established murine model of MI, obtained via permanent ligation of the left anterior descending coronary artery, we tested our hypothesis by measuring in primary isolated fibroblasts and cardiosomes the expression levels of a set of miRNAs, which we found to be upregulated in cardiomyocytes post-MI and to be involved in myofibroblast phenoconversion. Results Bioinformatic studies validated by biological assays identified three cardiomyocyte-specific miRNAs (namely miR-92a, miR-195, and miR-494) that are upregulated following cardiac ischemia and are also known to regulate α-SMA expression. We demonstrated that these miRNAs are upregulated in fibroblasts post-ischemia and are also contained in cardiosomes; to ensure that these miRNAs were confined inside cardiosomes, the samples were treated with RNase, showing that the level of miRNAs was not affected by RNase treatment, unless in presence of the detergent Triton X-100. The activation of myofibroblasts was confirmed by the increased expression of α-SMA. Using a luciferase assay, we also validated that miR-92a, miR-195, and mir-494 target the 3'UTR of α-SMA and regulate its transcription. Moreover, we observed that primary isolated cardiac fibroblasts were activated both when incubated with cardiosomes isolated from ischemic cardiomyocytes and when cultured in conditioned medium of post-MI cardiomyocytes, whereas no significant effects were detected following incubation with cardiosomes or medium from sham cardiomyocytes. Strikingly, myofibroblast phenoconversion was markedly attenuated when GW4869, an inhibitor of neutral sphingomyelinase 2 responsible for cardiosomes secretion, was added to cultured post-MI cardiomyocytes. Conclusion Taken together, our findings indicate that three cardiomyocyte-specific miRNAs (miR-92a, miR-195, and miR-494) are crucial in the activation of myofibroblasts." @default.
• W2981736579 created "2019-11-01" @default.
• W2981736579 creator A5019034390 @default.
• W2981736579 creator A5036945888 @default.
• W2981736579 creator A5064879576 @default.
• W2981736579 creator A5088545874 @default.
• W2981736579 date "2019-10-01" @default.
• W2981736579 modified "2023-10-17" @default.
• W2981736579 title "P2587Cardiosomal microRNAs are essential in post-infarction myofibroblast phenoconversion" @default.
• W2981736579 doi "https://doi.org/10.1093/eurheartj/ehz748.0913" @default.
• W2981736579 hasPublicationYear "2019" @default.
• W2981736579 type Work @default.
• W2981736579 sameAs 2981736579 @default.
• W2981736579 citedByCount "0" @default.
• W2981736579 crossrefType "journal-article" @default.
• W2981736579 hasAuthorship W2981736579A5019034390 @default.
• W2981736579 hasAuthorship W2981736579A5036945888 @default.
• W2981736579 hasAuthorship W2981736579A5064879576 @default.
• W2981736579 hasAuthorship W2981736579A5088545874 @default.
• W2981736579 hasConcept C104317684 @default.
• W2981736579 hasConcept C127561419 @default.
• W2981736579 hasConcept C142724271 @default.
• W2981736579 hasConcept C145059251 @default.
• W2981736579 hasConcept C164705383 @default.
• W2981736579 hasConcept C20518536 @default.
• W2981736579 hasConcept C207865475 @default.
• W2981736579 hasConcept C2780559512 @default.
• W2981736579 hasConcept C502942594 @default.
• W2981736579 hasConcept C541997718 @default.
• W2981736579 hasConcept C54355233 @default.
• W2981736579 hasConcept C60644358 @default.
• W2981736579 hasConcept C71924100 @default.
• W2981736579 hasConcept C86803240 @default.
• W2981736579 hasConcept C95444343 @default.
• W2981736579 hasConceptScore W2981736579C104317684 @default.
• W2981736579 hasConceptScore W2981736579C127561419 @default.
• W2981736579 hasConceptScore W2981736579C142724271 @default.
• W2981736579 hasConceptScore W2981736579C145059251 @default.
• W2981736579 hasConceptScore W2981736579C164705383 @default.
• W2981736579 hasConceptScore W2981736579C20518536 @default.
• W2981736579 hasConceptScore W2981736579C207865475 @default.
• W2981736579 hasConceptScore W2981736579C2780559512 @default.
• W2981736579 hasConceptScore W2981736579C502942594 @default.
• W2981736579 hasConceptScore W2981736579C541997718 @default.
• W2981736579 hasConceptScore W2981736579C54355233 @default.
• W2981736579 hasConceptScore W2981736579C60644358 @default.
• W2981736579 hasConceptScore W2981736579C71924100 @default.
• W2981736579 hasConceptScore W2981736579C86803240 @default.
• W2981736579 hasConceptScore W2981736579C95444343 @default.
• W2981736579 hasLocation W29817365791 @default.
• W2981736579 hasOpenAccess W2981736579 @default.
• W2981736579 hasPrimaryLocation W29817365791 @default.
• W2981736579 hasRelatedWork W1093472 @default.
• W2981736579 hasRelatedWork W16620575 @default.
• W2981736579 hasRelatedWork W18079785 @default.
• W2981736579 hasRelatedWork W18636367 @default.
• W2981736579 hasRelatedWork W2242183 @default.
• W2981736579 hasRelatedWork W3021762 @default.
• W2981736579 hasRelatedWork W6668492 @default.
• W2981736579 hasRelatedWork W7903652 @default.
• W2981736579 hasRelatedWork W9486145 @default.
• W2981736579 hasRelatedWork W18882737 @default.
• W2981736579 isParatext "false" @default.
• W2981736579 isRetracted "false" @default.
• W2981736579 magId "2981736579" @default.
• W2981736579 workType "article" @default.