LncRNA SNHG1 promotes the development of preeclampsia by interacting with PTBP1 and modulating NGFR mRNA stability.

BACKGROUND

Preeclampsia (PE) is a serious complication of pregnancy associated with trophoblast dysfunction accompanied by lncRNA dysregulation. This study investigated the functions of lncRNA SNHG1 in PE pathogenesis.

METHODS

Differentially expressed genes were identified in the GEO GSE102897 dataset. Twenty pairs of placental tissue samples and clinical data were collected from patients with PE and those with normal pregnancies. SNHG1 expression was measured using qPCR, and its associations with clinical parameters were analyzed. The effects of SNHG1 overexpression and knockdown were examined in HTR-8/SVneo trophoblast cells, and functional assays (including CCK-8, EdU, flow cytometry, and Transwell assays) were used to examine the effects of SNHG1 on trophoblast proliferation, apoptosis, migration, and invasion. Bioinformatics prediction and molecular biology experiments (such as RIP, RNA-seq, and Western blotting) were used to identify and verify the SNHG1-binding protein PTBP1 and its target gene NGFR.

RESULTS

Significant downregulation of lncRNA SNHG1 was observed in PE placental tissues from the GEO dataset, and SNHG1 levels were negatively correlated with blood pressure readings. SNHG1 knockdown inhibited trophoblast proliferation, migration, and invasion while promoting apoptosis, whereas overexpression had the opposite effects. SNHG1 was localized in the cytoplasm, where its downregulation enhanced the stability of nerve growth factor receptor (NGFR) mRNA and upregulated NGFR expression by binding with polypyrimidine tract-binding protein 1 (PTBP1), influencing trophoblast proliferation and apoptosis.

CONCLUSION

SNHG1 regulates trophoblast function through the SNHG1/PTBP1/NGFR axis, contributing to PE pathogenesis. The results provide novel theoretical insights and potential therapeutic targets for PE treatment.