Cell Journal (Apr 2024)

Increased Gene Expression of LITAF, TNF-α and BCL6 in Endometrial Tissues of Women with Endometriosis: A Case-Control Study

  • Ameneh Saadat Varnosfaderani,
  • Shadi Kalantari,
  • Fariba Ramezanali,
  • Maryam Shahhoseini,
  • Elham Amirchaghmaghi

DOI
https://doi.org/10.22074/cellj.2024.2022348.1503
Journal volume & issue
Vol. 26, no. 4
pp. 243 – 249

Abstract

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Objective: Endometriosis, as a common inflammatory chronic disease is characterized by endometrial tissue growthoutside the uterine cavity. It was reported that lipopolysaccharides (LPS) activate a transcription factor called LPSinduced tumor necrosis factor-alpha (LITAF) in macrophages, which induced transcription of cytokine genes suchas tumor necrosis factor alpha (TNF-α). B-cell lymphoma 6 protein (BCL6) is a transcription factor which expressionwas increased in endometrial tissues of infertile women with endometriosis. In addition, it was shown that mRNA andprotein of LITAF and BCL6 were inversely related in mature B lymphocytes and B-Cell lymphomas. Accordingly, weinvestigated gene expression of LITAF, BCL6 and TNF-α in eutopic and ectopic endometrial tissues of women withendometriosis compared to the controls.Materials and Methods: In this case-control study, 10 women with endometriosis (endometriosis group) and 10 women without endometriosis (control group) enrolled after diagnostic laparoscopy. Real-time polymerase chain reaction (PCR) technique was used to quantitatively analyze gene expression. One-Way ANOVA was used for data analysis.Results: This study showed that LITAF gene expression was significantly higher in ectopic endometrial tissuescompared to the control samples. Expression level of BCL6 gene was significantly increased in the ectopic tissuesof women with endometriosis compared to the control and eutopic samples. Although TNF-ɑ gene expression wasincreased in the ectopic lesions compared to the eutopic and control endometrial samples, these differences were notsignificant.Conclusion: The results suggested that over-expression of these inflammatory genes in ectopic endometrial lesionscan be considered as a molecular scenario in pathophysiology of endometriosis by induction of inflammatory cascades and cellular proliferation.

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