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Updated: Dec 19, 2025

Isolation of Primary Mouse Trophoblast Cells and Trophoblast Invasion Assay
Published on: January 8, 2012
MiR-384 inhibits proliferation and migration of trophoblast cells via targeting PTBP3
Wenbo Zhou1, Guangtong She1, Kaiyan Yang1
1Changzhou Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Changzhou 213003, Jiangsu, China.
Preeclampsia (PE) is one type of hypertension during pregnancy that seriously threatens maternal and infant health. Trophoblast dysfunction, such as decreased proliferation and migration, is closely related to the occurrence and development of PE. MicroRNAs (miRNAs) have been proven to play an important role in many diseases, including PE. miR-384 was reported to play a regulatory role in promoting cell apoptosis and inhibiting proliferation, migration and invasion in a variety of tumors. Previously, we found that miR-384 is upregulated in the placenta and plasma in the context of PE. In this study, we elucidated the function of miR-384 in the trophoblast cell line HTR-8/SVneo and the trophoblastic tumor cell line JEG-3. Cell proliferation and migration were inhibited by miR-384 overexpression but promoted by miR-384 downregulation. Subsequently, polypyrimidine tract-binding protein 3(PTBP3) was found to be a direct target gene of miR-384. PTBP3 was downregulated in placental tissues from PE patients, and a negative correlation was found between PTBP3 and miR-384. Our results suggest that the miR-384/PTBP3 axis plays an important role in regulating trophoblast function during the progression of PE, and these data provide novel insight into the molecular pathogenesis of this disorder.
Preeclampsia (PE) is one type of hypertension during pregnancy that seriously threatens maternal and infant health. Trophoblast dysfunction, such as decreased proliferation and migration, is closely related to the occurrence and development of PE. MicroRNAs (miRNAs) have been proven to play an important role in many diseases, including PE. miR-384 was reported to play a regulatory role in promoting cell apoptosis and inhibiting proliferation, migration and invasion in a variety of tumors. Previously, we found that miR-384 is upregulated in the placenta and plasma in the context of PE. In this study, we elucidated the function of miR-384 in the trophoblast cell line HTR-8/SVneo and the trophoblastic tumor cell line JEG-3. Cell proliferation and migration were inhibited by miR-384 overexpression but promoted by miR-384 downregulation. Subsequently, polypyrimidine tract-binding protein 3(PTBP3) was found to be a direct target gene of miR-384. PTBP3 was downregulated in placental tissues from PE patients, and a negative correlation was found between PTBP3 and miR-384. Our results suggest that the miR-384/PTBP3 axis plays an important role in regulating trophoblast function during the progression of PE, and these data provide novel insight into the molecular pathogenesis of this disorder.
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