http://purl.uniprot.org/citations/28453731 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/28453731 | http://www.w3.org/2000/01/rdf-schema#comment | "AimsVessel maturation involves the recruitment of mural cells such as pericytes and smooth muscle cells. Laminar shear stress is a major trigger for vessel maturation, but the molecular mechanisms by which shear stress affects recruitment of pericytes are unclear. MicroRNAs (miRs) are small non-coding RNAs, which post-transcriptionally control gene expression. The aim of the present study was to unveil the mechanism by which shear stress-regulated microRNAs contribute to vessel maturation.Methods and resultsHere, we show that laminar shear stress increased miR-27a and miR-27b expression in vitro and in ex vivo in mouse femoral artery explants. Overexpression of miR-27b in endothelial cells increased pericyte adhesion and pericyte recruitment in vitro. In vitro barrier function of endothelial-pericyte co-cultures was augmented by miR-27b overexpression, whereas inhibition of miR-27a/b reduced adhesion and pericyte coverage and decreased barrier functions. In vivo, pharmacological inhibition of miR-27a/b by locked nucleic acid antisense oligonucleotides significantly reduced pericyte coverage and increased water content in the murine uterus. MiR-27b overexpression repressed semaphorins (SEMA), which mediate repulsive signals, and the vessel destabilizing human but not mouse Angiopoietin-2 (Ang-2). Silencing of SEMA6A and SEMA6D rescued the reduced pericyte adhesion by miR-27 inhibition. Furthermore, inhibition of SEMA6D increased barrier function of an endothelial-pericyte co-culture in vitro.ConclusionThe present study demonstrates for the first time that shear stress-regulated miR-27b promotes the interaction of endothelial cells with pericytes, partly by repressing SEMA6A and SEMA6D."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.org/dc/terms/identifier | "doi:10.1093/cvr/cvx032"xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Hecker M."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Liebner S."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Stark K."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Dimmeler S."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Massberg S."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Lucas T."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Korff T."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Doddaballapur A."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Kaluza D."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Zehendner C.M."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Devraj K."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Eckart A."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Boon R.A."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Manavski Y."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/author | "Demolli S."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/name | "Cardiovasc Res"xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/pages | "681-691"xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/title | "Shear stress-regulated miR-27b controls pericyte recruitment by repressing SEMA6A and SEMA6D."xsd:string |
http://purl.uniprot.org/citations/28453731 | http://purl.uniprot.org/core/volume | "113"xsd:string |
http://purl.uniprot.org/citations/28453731 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28453731 |
http://purl.uniprot.org/citations/28453731 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/28453731 |