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Forkhead Box P3 Methylation and Expression in Men with Obstructive Sleep Apnea
David Sanz-Rubio1, Arianne Sanz2, Luis Varona3
1Translational Research Unit, Hospital Universitario Miguel Servet, Instituto de Investigación Sanitaria de Aragón (IISAragón), 50009 Zaragoza, Spain.
International Journal of Molecular Sciences
|March 27, 2020
Summary
Epigenetic changes in obstructive sleep apnea (OSA) are not linked to the FOXP3 gene in adults. This study found no differences in FOXP3 methylation or expression in adults with OSA, regardless of inflammation levels.
Area of Science:
- Immunogenetics
- Sleep Medicine
- Epigenetics
Background:
- Epigenetic alterations in obstructive sleep apnea (OSA) may explain end-organ damage.
- In children with OSA, Forkhead Box P3 (FOXP3) DNA methylation correlated with inflammatory markers.
- However, FOXP3 methylation patterns and their impact on gene expression in adults with OSA remain uninvestigated.
Purpose of the Study:
- To investigate the methylation status and expression of the FOXP3 gene in adults with obstructive sleep apnea (OSA).
- To determine if FOXP3 epigenetic modifications are associated with inflammation in adult OSA patients.
Main Methods:
- Analysis of plasma samples from adult patients with severe OSA and matched controls (EPIOSA Study).
- Evaluation of FOXP3 gene promoter and Treg-specific demethylated region (TSDR) methylation via PCR and pyrosequencing.
- Quantification of FOXP3 protein and mRNA expression using ELISA and qRT-PCR, alongside assessment of C-reactive protein (CRP) and Treg cells.
Main Results:
- No significant differences in FOXP3 promoter or TSDR methylation were observed between OSA patients and controls.
- FOXP3 protein and mRNA expression levels were comparable in both groups, irrespective of CRP levels.
- No association was found between FOXP3 methylation/expression and inflammatory status in adult OSA.
Conclusions:
- FOXP3 gene methylation is not altered in adults suffering from obstructive sleep apnea.
- FOXP3 gene expression remains unchanged in adult OSA patients, independent of their inflammatory status.
- These findings suggest FOXP3 epigenetic regulation is not a significant factor in adult OSA pathophysiology.
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