Aberrant expression of BAX, MEG3, and miR-214-3P genes in recurrent pregnancy loss

  • Saja Al-Rubaye
  • Sayyed Mohammad Hossein Ghaderian
  • Saghar Salehpour
  • Tayyebali Salmani
  • Samaneh Vojdani
  • Rusul Yaseen
  • Reza Akbarzadeh

Abstract

AIMS: Recurrent pregnancy loss (RPL), with unknown causes, is one of the most common challenges facing pregnancy. Apoptotic signaling pathways are involved in the normal and abnormal pregnancy process. Despite the evidence pointing toward the aberrant expression of apoptotic and apoptotic-related genes in pregnancy complications, the involvement of these genes in RPL remains to be elucidated. This study aimed to investigate the expression levels of BAX, MEG3, and miR-214-3p (as a microRNA), and their associations in an Iranian population.

MATERIALS AND METHODS: Following the extraction of RNA from blood samples of RPL patients and controls, quantitative expression levels of BAX, MEG3, and miR-214-3p genes were analyzed by real-time RT-PCR.

RESULTS: The findings showed that the expression levels of BAX and miRNA-214-3p were significantly higher in the blood samples of RPL patients than in control samples. In contrast, the expression of MEG3 was significantly down-regulated in women RPL. Furthermore, altered expressions of MEG3 and miRNA-214-3p are associated with their target gene BAX, where the BAX expression is positively and negatively correlated with the expressions of has-miR-214-3P and MEG3, respectively. ROC curve evaluation demonstrated the highest specificity and diagnostic value for miR-214-3p expression in distinguishing RPL samples from the healthy controls.

CONCLUSIONS: These data indicated that the aberrant expression of BAX, MEG3, miRNA-214-3p genes in RPL patients could provide new insights into the biological characteristics and related pathways of differentially expressed genes, which could help as potential diagnostic biomarkers and a better understanding of the molecular mechanisms of RPL.

Bibliographical data

Original languageEnglish
ISSN0951-3590
DOIs
Publication statusPublished - 07.2021
Externally publishedYes
PubMed 33719810