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Antiphospholipid antibody-induced miR-146a-3p drives trophoblast interleukin-8 secretion through activation of Toll-like receptor 8

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Gysler, Stefan M., Mulla, Melissa J., Guerra, Marta, Brosens, Jan J., Salmon, Jane E., Chamley, Lawrence W. and Abrahams, Vikki M. (2016) Antiphospholipid antibody-induced miR-146a-3p drives trophoblast interleukin-8 secretion through activation of Toll-like receptor 8. Molecular Human Reproduction, 22 (7). pp. 465-474. doi:10.1093/molehr/gaw027 ISSN 1360-9947.

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Official URL: http://dx.doi.org/10.1093/molehr/gaw027

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Abstract

STUDY QUESTION
What is the role of microRNAs (miRs) in antiphospholipid antibody (aPL)-induced trophoblast inflammation?

SUMMARY ANSWER
aPL-induced up-regulation of trophoblast miR-146a-3p is mediated by Toll-like receptor 4 (TLR4), and miR-146a-3p in turn drives the cells to secrete interleukin (IL)-8 by activating the RNA sensor, TLR8.

WHAT IS KNOWN ALREADY
Obstetric antiphospholipid syndrome (APS) is an autoimmune disorder characterized by circulating aPL and an increased risk of pregnancy complications. We previously showed that aPL recognizing beta2 glycoprotein I (β2GPI) elicit human first trimester trophoblast secretion of IL-8 by activating TLR4. Since some miRs control TLR responses, their regulation in trophoblast cells by aPL and functional role in the aPL-mediated inflammatory response was investigated. miRs can be released from cells via exosomes, and therefore, miR exosome expression was also examined. A panel of miRs was selected based on their involvement with TLR signaling: miR-9; miR-146a-5p and its isomiR, miR-146a-3p; miR-155, miR-210; and Let-7c. Since certain miRs can activate the RNA sensor, TLR8, this was also investigated.

Item Type: Journal Article
Divisions: Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Clinical Trials Unit
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School
Journal or Publication Title: Molecular Human Reproduction
Publisher: Oxford University Press
ISSN: 1360-9947
Official Date: 1 July 2016
Dates:
DateEvent
1 July 2016Published
12 July 2016Available
23 March 2016Accepted
Volume: 22
Number: 7
Page Range: pp. 465-474
DOI: 10.1093/molehr/gaw027
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Open Access (Creative Commons)

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