Roles of microRNA-34a in the pathogenesis of placenta accreta
Article first published online: 4 JUN 2012
© 2012 The Authors. Journal of Obstetrics and Gynaecology Research © 2012 Japan Society of Obstetrics and Gynecology
Journal of Obstetrics and Gynaecology Research
Volume 39, Issue 1, pages 67–74, January 2013
How to Cite
Umemura, K., Ishioka, S.-i., Endo, T., Ezaka, Y., Takahashi, M. and Saito, T. (2013), Roles of microRNA-34a in the pathogenesis of placenta accreta. Journal of Obstetrics and Gynaecology Research, 39: 67–74. doi: 10.1111/j.1447-0756.2012.01898.x
- Issue published online: 7 JAN 2013
- Article first published online: 4 JUN 2012
- Received date: August 26 2011.; Accepted date: February 8 2012.
- fluorescent in situ hybridization;
- placenta accreta;
- plasminogen activator inhibitor-1
Aim: MicroRNA-34a (miR-34a) is associated with invasion and metastasis of various cancers. The trophoblastic cells of placenta accreta invade into the myometrium in a similar way to the invasion of cancers. We studied the roles of miR-34a in the pathogenesis of placenta accreta.
Methods: The human choriocarcinoma cell line JAR was used for in vitro experiments as a model of trophoblasts, and placental tissues from the operative specimen of patients with or without placenta accreta were used for experiments in vivo. Morpholino antisense oligomer against miR-34a (miR-34a Morpho/AS) was added to JAR, and the expression of miR-34a and plasminogen activator inhibitor-1 (PAI-1) was determined by real time PCR. The effects of antisense, interleukin (IL)-6 and IL-8 in the process of invasion were studied with an invasion assay. Expression of miR-34a in vivo was studied with the use of fluorescent in situ hybridization (FISH).
Results: Expression of miR-34a was inhibited by 65% with the administration of antisense, and a slight increase in miR-34a expression was observed with the addition of IL-6 and IL-8. PAI-1 expression decreased with the addition of IL-6 and IL-8, and increased with the administration of antisense. There was an increase in invasive capacity through the inhibition of miR-34a expression. Strong FISH expression of miR-34a was observed in trophoblast cells of non-placenta accreta, and a clear decrease in miR-34a expression was observed in those of placenta accreta.
Conclusions: Expression of miR-34a was downregulated in placenta accreta. In vitro experiments also showed that the invasive potential of JAR increased by suppressing miR-34a, probably through the expression of PAI-1.