%0 Journal Article
%T Increased Gene Expression of LITAF, TNF-α and BCL6 in Endometrial Tissues of Women with Endometriosis: A Case-Control Study.
%A Varnosfaderani AS
%A Kalantari S
%A Ramezanali F
%A Shahhoseini M
%A Amirchaghmaghi E
%J Cell J
%V 26
%N 4
%D 2024 May 7
%M 38736408
%F 3.128
%R 10.22074/cellj.2024.2022348.1503
%X OBJECTIVE: Endometriosis, as a common inflammatory chronic disease is characterized by endometrial tissue growth outside 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 such as tumor necrosis factor alpha (TNF-α). B-cell lymphoma 6 protein (BCL6) is a transcription factor which expression was increased in endometrial tissues of infertile women with endometriosis. In addition, it was shown that mRNA and protein of LITAF and BCL6 were inversely related in mature B lymphocytes and B-Cell lymphomas. Accordingly, we investigated gene expression of LITAF, BCL6 and ,TNF-α in eutopic and ectopic endometrial tissues of women with endometriosis compared to the controls.
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 tissues compared to the control samples. Expression level of BCL6 gene was significantly increased in the ectopic tissues of women with endometriosis compared to the control and eutopic samples. Although TNF-ɑ gene expression was increased in the ectopic lesions compared to the eutopic and control endometrial samples, these differences were not significant.
CONCLUSIONS: The results suggested that over-expression of these inflammatory genes in ectopic endometrial lesions can be considered as a molecular scenario in pathophysiology of endometriosis by induction of inflammatory cascades and cellular proliferation.