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Autor(en) / Beteiligte
Titel
hsa-miR-320d and hsa-miR-582, miRNA biomarkers of aortic dissection regulate apoptosis of vascular smooth muscle cells
Ist Teil von
  • Journal of cardiovascular pharmacology, 2018-05, Vol.71 (5), p.275-282
Ort / Verlag
United States: Copyright Wolters Kluwer Health, Inc. All rights reserved
Erscheinungsjahr
2018
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • ABSTRACTAbnormal expression of microRNAs (miRNAs) has been associated with aortic dissection (AD). Next generation sequencing was performed to identify the differentially expressed miRNAs in aortic tissue samples between AD and non-diseased individuals. Selected miRNAs which showed significant variation between the two groups, were then transfected into human aortic vascular smooth muscle cells (HA-VSMC), and assessed for effects on cell migration and induced apoptosis. The changes in gene expression pattern in HA-VSMC cells transfected with the miRNAs were also investigated.Among the 314 miRNAs detected in the aortic tissues from both AD and normal subjects, 46 showed significantly different expression patterns. Only seven of these differentially expressed miRNAs were found to be enriched in AD, while the majority had diminished. Hsa-miR-320d and hsa-miR-582 were two representative miRNAs that exhibited a decrease of greater than 10-fold. Transfection of hsa-miR-320d and hsa-miR-582 did not affect the migration capability of the vascular smooth muscle cells, but remarkably enhanced the staurosporine and TNFα induced apoptosis, by 15% and 29% respectively. Furthermore, the transfection of both miRNAs affected the expression of a vast multitude of genes, majority of which were related to apoptotic pathways. The fluorescence reporter assays demonstrated that hsa-miR-320d and hsa-miR-582 bind the 3’ UTR region of TRIAP1 and NET1 genes, respectively. These results suggest that hsa-miR-320d and hsa-miR-582 may serve as putative biomarkers for AD research.
Sprache
Englisch
Identifikatoren
ISSN: 0160-2446
eISSN: 1533-4023
DOI: 10.1097/FJC.0000000000000568
Titel-ID: cdi_proquest_miscellaneous_2014144340
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