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10.1186/s11658-018-0091-3

http://scihub22266oqcxt.onion/10.1186/s11658-018-0091-3
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suck abstract from ncbi


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pmid29785186      Cell+Mol+Biol+Lett 2018 ; 23 (ä): ä
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  • Platelets activated by the anti-?2GPI/?2GPI complex release microRNAs to inhibit migration and tube formation of human umbilical vein endothelial cells #MMPMID29785186
  • Zhang Y; Zhang W; Zha C; Liu Y
  • Cell Mol Biol Lett 2018[]; 23 (ä): ä PMID29785186show ga
  • Background: Patients with anti-?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-?2GPI antibodies remains unknown. Methods: In this study, we derived miR-96 and -26a from platelets activated by the anti-?2GPI/?2GPI complex and explored their role in modulating human umbilical vein endothelial cell (HUVEC) migration and tube formation. Results: Anti-?2GPI/?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 miR-96 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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