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Updated: May 16, 2026
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Derivation of Mouse Trophoblast Stem Cells from Blastocysts
Published on: June 8, 2010
METTL14 promotes trophoblast dysfunction by elevating SZRD1 expression in an m6A-dependent manner.
1Department of Obstetrics, The First Hospital of Putian City, Putian City, 353400, Fujian Province, China.
Human Cell
|May 14, 2026
Summary
Preeclampsia involves increased SUZ RNA binding domain containing 1 (SZRD1) and Methyltransferase-like 14 (METTL14) expression. Targeting this METTL14/SZRD1 axis may offer a new therapeutic strategy for preeclampsia.
Area of Science:
- Obstetrics and Gynecology
- Molecular Biology
- Genetics
Background:
- Preeclampsia is a major cause of maternal and perinatal mortality.
- Altered gene expression is implicated in preeclampsia pathogenesis.
- The role of SUZ RNA binding domain containing 1 (SZRD1) in preeclampsia remains unclear.
Purpose of the Study:
- To investigate the expression and function of SZRD1 in preeclampsia.
- To elucidate the molecular mechanism underlying SZRD1's role in preeclampsia.
- To explore the potential of the METTL14/SZRD1 axis as a therapeutic target.
Main Methods:
- Gene expression analysis using RT-qPCR and Western blot.
- In vitro assessment of trophoblast cell function (proliferation, apoptosis, migration, invasion, angiogenesis).
- Analysis of METTL14 and SZRD1 interaction using MeRIP-qPCR and RIP assays.
Main Results:
- SZRD1 and METTL14 were significantly upregulated in preeclamptic placentas.
- SZRD1 silencing promoted trophoblast cell proliferation, migration, invasion, and angiogenesis while inhibiting apoptosis.
- METTL14 enhanced SZRD1 mRNA stability through m6A methylation, exacerbating trophoblast dysfunction.
Conclusions:
- The METTL14/SZRD1 axis plays a critical role in preeclampsia pathogenesis.
- METTL14-mediated stabilization of SZRD1 contributes to trophoblast dysfunction.
- Targeting the METTL14/SZRD1 pathway presents a potential therapeutic avenue for preeclampsia.
