Association of lncRNA SH3PXD2A-AS1 with preeclampsia and its function in invasion and migration of placental trophoblast cells

Cell Death Dis. 2020 Jul 27;11(7):583. doi: 10.1038/s41419-020-02796-0.

Abstract

Accumulating evidence suggests that the pathogenesis of preeclampsia involves poor placentation caused by insufficient trophoblast invasion and impaired uterine spiral artery remodeling, yet the underlying molecular mechanism remains unclear. We carried out transcriptome profiling on placentae from preeclamptic patients and normal subjects, and identified about four hundred long non-coding RNAs differentially expressed in placentae of patients with early-onset severe preeclampsia. Here, we report our identification of lncRNA SH3PXD2A-AS1 as a potential causal factor for this disease and its downstream pathways involved in placentation. We found that expression level of SH3PXD2A-AS1 in the placentae is positively correlated with clinical severity of the patients. We demonstrated that SH3PXD2A-AS1 inhibited invasion and migration through recruiting CCCTC-binding factor (CTCF) to the promoters of SH3PXD2A and CCR7 to inhibit their transcription. Therefore, we conclude that the upregulation of lncRNA SH3PXD2A-AS1 may contribute to the pathogenesis of preeclampsia through prohibiting trophoblast invasion during placentation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • CCCTC-Binding Factor / metabolism
  • Cell Cycle Checkpoints / genetics
  • Cell Death / genetics
  • Cell Line
  • Cell Movement / genetics*
  • Cell Proliferation / genetics
  • Female
  • Humans
  • Placenta / pathology*
  • Pre-Eclampsia / genetics*
  • Pre-Eclampsia / pathology
  • Pregnancy
  • Promoter Regions, Genetic / genetics
  • Protein Binding
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • Receptors, CCR7 / metabolism
  • Subcellular Fractions / metabolism
  • Transcription, Genetic
  • Trophoblasts / metabolism*
  • Trophoblasts / pathology*
  • Up-Regulation / genetics

Substances

  • CCCTC-Binding Factor
  • CCR7 protein, human
  • CTCF protein, human
  • RNA, Long Noncoding
  • Receptors, CCR7