AI Article Synopsis
- Preeclampsia (PE) is a serious condition that can happen during pregnancy and is linked to inflammation and problems with certain cells in the body.
- Researchers studied a specific RNA called HOXD-AS1 and found it plays a role in PE by affecting levels of other molecules and influencing inflammation.
- The findings suggest that targeting HOXD-AS1 and its interactions with other parts of the cell could help understand and maybe treat PE better.
Article Abstract
Background: Preeclampsia (PE) is a serious pregnancy-specific syndrome associated with the inadequate invasion of trophoblast cells and inflammation of the uterus. A previous study found that lncRNA HOXD-AS1 promotes PE. However, its regulatory network requires additional exploration.
Methods: HOXD-AS1-targeted miRNAs and genes were predicted by different databases in a bioinformatics analysis. The expression HOXD-AS1 and its potential mA methylase (METTL3) were detected in placentas from healthy female patients with PE. The targeting relationship and role of the HOXD-AS1/miR-135a/β-TRCP axis in trophoblast cells were demonstrated by overexpression/knockdown assays. The levels of β-TRCP downstream pathway proteins IκBα, NF-κB, and p65 were measured. The levels of inflammatory factors in cell supernatants were detected by ELISA. To verify the molecular mechanism of β-TRCP in PE, IκBα was co-overexpressed in β-TRCP in trophoblast cells.
Results: The levels of METTL3, HOXD-AS1, and β-TRCP were elevated in PE placental tissues, while miR-135a levels were reduced. MiR-135a was found to be targeted by HOXD-AS1, and HOXD-AS1 expression was maintained at a high level by METTL3-mediated mA methylation. Overexpression of METTL3, HOXD-AS1, and β-TRCP, and knockdown of miR-135a in HTR-8/SVneo cells all inhibited cell invasion and migration, and promoted apoptosis and the secretion of inflammatory factors. Knockdown of METTL3, HOXD-AS1, and β-TRCP, and overexpression of miR-135a had the opposite effects. Furthermore, IκBα expression was negatively associated with β-TRCP expression, and the levels of NF-κB, p65, and NLRP3 were positively regulated by β-TRCP. A high level of β-TRCP expression attenuated the effect of HOXD-AS1 knockdown in trophoblast cells.
Conclusion: METTL3 functioned to maintain a high level of HOXD-AS1 expression in PE, which influenced inflammation and the migration and invasion of trophoblast cells via the miR-135a/β-TRCP axis and NF-κB pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10700154 | PMC |
| http://dx.doi.org/10.1016/j.ncrna.2023.11.006 | DOI Listing |
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