Abstract
Background:
The objective was to elucidate the potential epigenetic regulatory mechanism in HMOX1 expression in preeclampsia.
Materials & methods:
HMOX1 promoter DNA methylation was evaluated in the placental tissue and blood of preeclamptic and normotensive pregnant women. HMOX1 and miR-153-3p gene expression were assessed in placental tissue and peripheral blood mononuclear cells (PBMCs). Related microarray datasets in the Gene Expression Omnibus database were also analyzed.
Results:
In placental tissue, despite HMOX1 expression downregulation, there was no significant change in HMOX1 methylation. In PBMCs, there was no significant alteration in HMOX1 expression, while hypomethylation was observed in blood. The miR-153-3p expression increased in the placental tissue and in the PBMCs of preeclampsia.
Conclusion:
DNA methylation does not affect HMOX1 expression, while miR-153-3p might be a biomarker for preeclampsia.
Tweetable abstract
In this study, by investigation of HMOX1 DNA methylation in placental tissue and blood, along with the potential regulatory role of miR-153-3p, the authors provided new insight into HMOX1 gene expression regulation and preeclampsia pathogenesis.
Supplementary data
To view the supplementary data that accompany this paper please visit the journal website at: www.tandfonline.com/doi/suppl/10.2217/epi-2023-0377
Author contributions
Z Rahimi, NA Rezvani, N Jalilian and S Rahimi designed the study. S Rahimi analyzed the data and wrote the manuscript. Z Rahimi and N Jalilian edited the manuscript. S Rahimi, NA Rezvani, S Khazayel and K Yari performed the experiments. S Rahimi and F Khadir collected the samples. Z Rahimi and E Shakiba supervised the project.
Acknowledgments
This work was performed in partial fulfillment of the requirements for the PhD degree of Somayeh Rahimi. The authors would like to extend their sincere gratitude to all the participants who generously contributed to this study.
Financial disclosure
This project was funded by the Vice Chancellor Office for Research of the Kermanshah University of Medical Sciences, Kermanshah, Iran (grant number: 990950).
Competing interests disclosure
The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.
Writing disclosure
No writing assistance was utilized in the production of this manuscript.
Ethical conduct of research
The Ethics Committee of the Kermanshah University of Medical Science granted approval for this study (approval ID: IR.KUMS.REC.1399.1079). All participants provided written consent after being fully informed.
Data sharing statement
The data that support the findings of this study are available from the corresponding author upon reasonable request. The data related to the insilico section of this study are publicly available on the Gene Expression Omnibus website (www.ncbi.nlm.nih.gov/geo/).