ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
RBM15/YTHDF2-mediated m6A modification of HTR1D exacerbates hypoxia-induced dysfunction in trophoblast cells in preeclampsia.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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5 authors.
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Abstract
backgroundPreeclampsia (PE), a hypertensive disorder of pregnancy, is characterized by impaired trophoblast cell function. The 5-hydroxytryptamine receptor 1D (HTR1D) has been implicated in trophoblast cell regulation, yet its specific role and the underlying molecular mechanisms in preeclampsia remain unclear.
methodsTrophoblast cells (HTR-8/SVneo) were exposed to CoCl
resultsHTR1D expression was significantly downregulated in PE patients and hypoxia-induced HTR-8/SVneo cells, whereas RBM15 expression was upregulated. Overexpression of HTR1D mitigated hypoxia-induced inhibition of trophoblast proliferation and migration, as well as reduced apoptosis and oxidative stress. RBM15 was found to destabilize HTR1D mRNA in a YTHDF2-dependent manner. Silencing RBM15 enhanced trophoblast proliferation and migration while suppressing apoptosis and oxidative stress by upregulating HTR1D.
conclusionThe RBM15/YTHDF2-mediated destabilization of HTR1D mRNA exacerbated hypoxia-induced dysfunction in trophoblast cells associated with PE. These findings highlight the potential of targeting the RBM15/HTR1D axis as a therapeutic strategy for managing PE.
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