YTHDF1 and YTHDF3 gene expression in coronary artery plaque

Creative Commons License

Arslan S., Özbilüm Şahin N., Tüzemen Bayyurt E. B., Aşam M., Yılmaz M. B.

10th molecular biology and biotechnology congress, Adana, Türkiye, 4 - 08 Ekim 2021, ss.70

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Adana
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.70
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

Coronary artery disease (CAD) is caused by plaque buildup in the wall of the coronary arteries that supply blood to the heart. Plaque is made up of cholesterol deposits. Plaque buildup causes the inside of the arteries to narrow over time. This process is called atherosclerosis. N6-Methyladenosine (m6A) is the most common RNA modification in eukaryotic messenger RNAs (mRNAs). m6A influences mRNA splicing, export, localization, translation, decay, and stability. m6A RNA modification is reversible and catalyzed by a recently discovered multicomponent protein complex, including methyltransferases, demethylases, and m6A binding proteins such as YTH N6-methyladenosine RNA binding protein 1 and 3 (YTHDF1 and YTHDF3). YTHDF1 and 3 are members of the YTH domaincontaining proteins. m6A mRNA methylation regulates cardiac gene expression. We compared YTHDF1 and YTHDF3 expression between coronary artery plaque and internal mammary artery (IMA-choice for coronary artery bypass grafting) in this study. We isolated total RNA from 38 tissue samples composed of 20 plaque and 18 IMA. Then we performed quantitative real time polymerase chain reaction (qRT-PCR) using syber green method. GAPDH was used as reference gene. YTHDF1 and YTHDF3 were upregulated 1.41 (p:0.11) and 1.15 fold (p:0.66), respectively in plaque tissue compared with control samples. As a result, YTHDF1-3 may have effective role RNA methylation process in coronary artery plaque formation. But further molecular function studies will need in future.