TGFB1 and TGFBR2 gene polymorphisms and pathophysiology of severe preeclampsia

نویسندگان

  • Anita Deborah Anwar
  • Firman Fuad Wirakusumah
  • Sofie Rifayani Krisnadi
چکیده

Transforming growth factor β1 (TGFB1) and transforming growth factor β type 2 receptor (TGFBR2) are key components of TGF-β signaling and play an important role in vascular remodeling in placentation. Several polymorphisms have been identified in TGFB1 and TGFBR2 genes, including those associated with the regulation of TGF-β1 levels and TGF binding to its receptor. The decrease of TGF-β1 levels and the disruption of TGF TGF-β1 signaling can cause abnormal placentation, hypoxia, and increased soluble endoglin (sEng), which can lead to preeclampsia.This study aims to determine the role of gene polymorphisms C-509T TGFB1 and C1167T TGFBR2and their relation to TGF-β1 and sEng levels in cases of severe preeclampsia. Genotyping performed using restriction fragment length polymorphism (RFLP) and a direct sequencing method was used to study 26 cases of preeclampsia against 26 control matched normal pregnancies. The results showed that the TGF-β1 levels in severe preeclampsia were significantly lower compared to normal pregnancies, whereas the levels of sEng in severe preeclampsia were significantly higher compared to normal pregnancies. In addition, the genotypes -509CT/TT TGFB1 and 1167CT/TT TGFBR2 appeared in both groups. This analysis highlights the absence of a significant association between the genotype -509C/T TGFB1 and TGF-β1 levels in both American Journal of Research Communication www.usa-journals.com Anwar, et al., 2015: 3(6) 29 [email protected] groups. The results did not indicate any significant associations between the genotypes 509C/T TGFB1 and 1167C/T TGFBR2 and the levels of sEng in both groups. Based on these results, it can be concluded that the levels of TGF-β1 and sEng are associated with severe preeclampsia but that the gene polymorphisms C-509T TGFB1 and C1167T TGFBR2 are not directly related to severe preeclampsia.

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تاریخ انتشار 2015