Journal
CELLULAR & MOLECULAR BIOLOGY LETTERS
Volume 23, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/s11658-018-0091-3
Keywords
Platelet-derived microparticles; MicroRNA; Endothelial cells
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Funding
- Young Natural Science Foundation of Heilongjiang Province [QC2010002]
- National Natural Science Foundation of China [81541031]
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Background: Patients with anti-beta 2GPI antibodies display significantly higher platelet activation/aggregation and vascular endothelial cell damage. The mechanism underlying the correlation between platelet activation, vascular endothelial cell dysfunctions and anti-beta 2GPI antibodies remains unknown. Methods: In this study, we derived miR-96 and -26a from platelets activated by the anti-beta 2GPI/beta 2GPI complex and explored their role in modulating human umbilical vein endothelial cell (HUVEC) migration and tube formation. Results: Anti-beta 2GPI/beta 2GPI complex induces the release of platelet-derived microparticles (p-MPs). The amounts of miR-96 and -26a in these p-MPs were also higher than for the control group. Co-incubation of HUVECs with p-MPs resulted in the transfer of miR96 and -26a into HUVECs, where they inhibited migration and tube formation. The targeting role of these miRNAs was further validated by directly downregulating targeted selectin-P (SELP) and platelet-derived growth factor receptor alpha (PDGFRA) via luciferase activity assay. Conclusion: Our study suggests that miR-96 and -26a in p-MPs can inhibit HUVEC behavior by targeting SELP and PDGFRA.
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