Vitamin D down-regulates microRNA-21 expression to promote human placental trophoblast cell migration and invasion .
10.12122/j.issn.1673-4254.2019.04.09
- Author:
Zhiyi ZHOU
1
;
Xiaojuan LI
1
;
Guoqing JIANG
1
;
Jue WANG
2
;
Yuan QIAN
2
Author Information
1. Department of Obstetrics First Affiliated Hospital of Kunming Medical University,, Kunming 650032, China.
2. Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
- Publication Type:Journal Article
- Keywords:
HTR-8/SVneo cells;
human placental trophoblast cells;
microRNA-21;
migration;
trophoblasts;
vitaminD
- MeSH:
Cell Movement;
Female;
Humans;
MicroRNAs;
genetics;
Placenta;
Pre-Eclampsia;
Pregnancy;
Trophoblasts;
Vitamin D
- From:
Journal of Southern Medical University
2019;39(4):437-442
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of vitamin D on microRNA-21(miR-21) expression and migration and invasion of human placental trophoblast cells.
METHODS:The changes in the expression of miR-21 were detected using RT-qPCR in HTR-8/SVneo cells following stimulation by vitamin D at different doses for 24, 48 and 72 h.HTR-8/SVneo cells transfected with miR-21 mimic or inhibitor with or without vitamin D treatment were examined for changes in cell migration and invasion abilities using Transwell assay, and Western blotting was used to detect protein expressions of E-cadherin, fibronectin, and MMP9.
RESULTS:Vitamin D obviously inhibited the expression of micoRNA-21 in HTR-8/SVneo cells in a concentration-and time-dependent manner.Transfection with the miR-21 mimic significantly inhibited the migration and invasion of HTR-8/SVneo cells, and this inhibitory effect was abolished by treatment with vitamin D; transfection with miR-21 inhibitor obviously promoted the migration and invasion of HTR-8/SVneo cells, and these effects were not significantly affected by vitamin D treatment.
CONCLUSIONS:Vitamin D may promote trophoblast cell migration and invasion to accelerate the development of preeclampsia by down-regulating the expression of miR-21.
