RESUMO
OBJECTIVE: MALAT1 has been confirmed to play a vital role in the progression of preeclampsia (PE). However, as one of the spliceosomes of MALAT1, the role and mechanism of MALAT1-201 in the progression of PE remain elusive. Mesenchymal stem cells (MSCs) correlate with angiogenesis and trophoblast formation and could maintain successful pregnancy, while the molecular mechanisms are still unclear. The aim of the study was to investigate the role and potential mechanism of MALAT1-201 in PE. METHODS: We isolated MSCs from bone marrow and cultured in vitro. We overexpressed MALAT1-201 in MSCs and collected exosomes released by MSCs to treat trophoblast cells. Then, the proliferation, apoptosis and migration of MALAT1-201 elevated trophoblast cells were detected by CCK-8, flow cytometer and transwell assay, respectively. The binding site between MALAT1-201 and miR-141 was detected by dual-luciferase assays. The location of MALAT1-201 was detected by cytoplasmic and nuclear RNA fractionation. RESULTS: We successfully cultured bone marrow derived MSCs in vitro. MSC-Ex carrying MALAT1-201 promoted proliferation and migration, while suppressed apoptosis of trophoblast cells, which is similar to the effects of MALAT1-201 gene on trophoblast cells. In addition, MALAT1-201 was mainly localized in the nucleus and miR-141 was the target of MALAT1-201. CONCLUSIONS: MALAT1-201 derived from MSC-Ex regulated the proliferation, apoptosis and migration of HTR8-Svneo cells by targeting miR-141, which indicated a promising therapeutic target for PE.
