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

• Published in: Cell death & disease Vol. 11; no. 7; p. 583
• Main Authors: Chen, Qian, Jiang, Sijia, Liu, Haihua, Gao, Yue, Yang, Xiaoxue, Ren, Zhonglu, Gao, Yunfei, Xiao, Lu, Hu, Haoyue, Yu, Yanhong, Yang, Xinping, Zhong, Mei
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 27.07.2020; Springer Nature B.V
• Subjects: 631/136/1425; 631/337/384; Adult; Age; Antibodies; Biochemistry; Biomedical and Life Sciences; CCCTC-Binding Factor - metabolism; CCR7 protein; Cell Biology; Cell Culture; Cell Cycle Checkpoints - genetics; Cell Death - genetics; Cell Line; Cell migration; Cell Movement - genetics; Cell Proliferation - genetics; Female; Gene expression; Humans; Immunology; Life Sciences; Non-coding RNA; Pathogenesis; Placenta; Placenta - pathology; Pre-eclampsia; Pre-Eclampsia - genetics; Pre-Eclampsia - pathology; Preeclampsia; Pregnancy; Promoter Regions, Genetic - genetics; Protein Binding; Receptors, CCR7 - metabolism; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Subcellular Fractions - metabolism; Transcription; Transcription, Genetic; Trophoblasts - metabolism; Trophoblasts - pathology; Up-Regulation - genetics; Uterus
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-020-02796-0

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.