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

The aim of the present study was to analyze the expression of the , , and genes, which participate in mechanisms related to the complex pathophysiology of endometriosis.  A case-control study was conducted with 40 women who were diagnosed with endometriosis, and 15 fertile and healthy women. Paired...

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Veröffentlicht in:Revista Brasileira de ginecologia e obstetrícia 2018-10, Vol.40 (10), p.606-613
Hauptverfasser: Gomes, Valéria Aguiar, Bonocher, Camila de Moraes, Rosa-E-Silva, Júlio César, de Paz, Cláudia Cristina Paro, Ferriani, Rui Alberto, Meola, Juliana
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Sprache:eng
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Zusammenfassung:The aim of the present study was to analyze the expression of the , , and genes, which participate in mechanisms related to the complex pathophysiology of endometriosis.  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 (  = 20) or secretory phases (  = 20) of the menstrual cycle. As controls, paired endometrial biopsy samples were collected from the healthy women in the proliferative (  = 15) and secretory (  = 15) phases of the same menstrual cycle. We analyzed the expression levels of the , , and genes by real-time polymerase chain reaction.  An increase in , , and 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.  These findings suggest that the , and 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.
ISSN:0100-7203
1806-9339
1806-9339
DOI:10.1055/s-0038-1673364