The Apoptotic, Angiogenic and Cell Proliferation Genes CD63, S100A6 e GNB2L1 are Altered in Patients with Endometriosis

Abstract

Objective The aim of the present study was to analyze the expression of the CD63, S100A6, and GNB2L1genes, which participate in mechanisms related to the complex pathophysiology of endometriosis. Methods A case-control study was conducted with 40 women who were diagnosed with endometriosis, and 15 fertile and healthy women. Paired samples of eutopic endometrium and endometriotic lesions (peritoneal and ovarian endometriotic implants) were obtained from the women with endometriosis in the proliferative (n = 20) or secretory phases (n = 20) of the menstrual cycle. As controls, paired endometrial biopsy samples were collected from the healthy women in the proliferative (n = 15) and secretory (n = 15) phases of the same menstrual cycle. We analyzed the expression levels of the CD63, S100A6, and GNB2L1 genes by real-time polymerase chain reaction. Results An increase in CD63, S100A6, and GNB2L1 gene transcript levels was observed in the ectopic implants compared with the eutopic endometrium of the women with and without endometriosis, regardless of the phase of the menstrual cycle. Conclusion These findings suggest that the CD63, S100A6, and GNB2L1 genes may be involved in the pathogenesis of endometriosis, since they participate in mechanisms such as inhibition of apoptosis, angiogenesis and cell proliferation, which lead to the loss of cell homeostasis in the ectopic endometrium, thus contributing to the implantation and survival of the tissue in the extrauterine environment.

Cellular Origins of Endometriosis: Towards Novel Diagnostics and Therapeutics

“…75 Briefly, they include members of the Wnt signaling pathway, 19,76,77 kinase signaling pathway, 78 micro-RNAs and long noncoding RNAs, 79 as well as cell adhesion molecules such as N-cadherin 54 and Claudin 11. 80 Furthermore, cellular functions such as enhanced cell survival (resistance to apoptosis; Tetraspanin-30), cell migration, angiogenesis, cellular proliferation, 81 and innervation 82,83 are thought to contribute to establishment of lesions. Cellular functions can also be modified by reproductive hormones 84 and conditions such as hypoxia, 85 resulting in an adhesive, and angiogenic phenotype.…”

Identification of Potential Molecular Mechanism Related to Infertile Endometriosis

“…The expression of GNB2L1 was higher in ectopic endometrial tissue from patients with endometriosis than in normal patients, regardless of whether they were in the proliferative or secretory phase of the menstrual cycle. GNB2L1 is associated with the progression of endometriosis and contributes to the removal of ectopic endometrium by reducing cell proliferation and angiogenesis ( 35 ). Therefore, GNB2L1 has the potential to act as a biomarker and therapeutic target for endometriosis.…”

An artificial neural network model based on autophagy-related genes in childhood systemic lupus erythematosus

“…DDIT3 is a multi-stress condition-induced transcription factor localized in the nucleus and cytoplasm, involved in regulating cell cycle arrest and apoptosis and has been shown to promote chondrocyte autophagy via the SIRT1-AKT pathway [28,29]. GNB2L1 functions in a variety of cellular activities and is involved in the recruitment, assembly and/or regulation of multiple signaling molecules [30]. CTSD, cathepsin D, is an acid protease that works on intracellular proteolysis and plays a dual role in cell proliferation and apoptosis [31].…”