BACKGROUND: Long noncoding RNAs play important roles in the development of various diseases. This study aimed to evaluate the effects and mechanism of VIM antisense RNA 1 (VIM-AS1) in the development of preeclampsia.

MATERIAL AND METHODS: HTR-8/SVneo cells were divided into normal control (NC), Model, Blank, and VIM-AS1 groups. These groups were analyzed for their VIM-AS1 gene expressions by RT-PCR, HTR-8/SVneo cell invasion was assessed by transwell and migration by wound healing, cell morphology was assessed by microscopy examination, and E-cadherin, Snail, and Vimentin genes expressions were assessed by RT-PCR and WB assay.

RESULTS: VIM-AS1 gene expression was significantly different among normal placenta tissue, mild preeclampsia tissues, and severe preeclampsia tissues (P<0.001 or P<0.01). VIM-AS1 gene expressions, cell invasions, and wound healing rates in the Model and Blank groups were significantly suppressed compared with that of NC group (P<0.001, all). With VIM-AS1 supplementation, VIM-AS1 gene expression, cell invasion, and wound healing rate in the VIM-AS1 group were significantly increased compared with that in the Model group (P<0.001). RT-PCR and WB assay showed that E-cadherin gene and protein expressions in Model and Blank groups were significantly upregulated compared with the NC group (P<0.001); Snail and Vimentin gene and protein expressions in the Model and Blank groups were significantly downregulated compared with the NC group (P<0.001). With VIM-AS1 supplementation, E-cadherin, Snail, and Vimentin gene and proteins expression levels in the VIM-AS1 group were significantly different compared with that in the Model group (P<0.001).

CONCLUSIONS: VIM-AS1 promotes preeclampsia via inducing epithelial-to-mesenchymal transition (EMT).

Keywords: Cadherins, enoxaparin, Pre-Eclampsia, Snails, Vimentin, Placenta, Pregnancy, RNA, Antisense