Expressions of Livin and Smac and their correlation in endometriosis

Abstract

Objective: To explore the expression of Livin (a new member of inhibitors of apoptosis proteins) and second mitochondriaderived activator of caspases (Smac) in endometriosis (EMs), and the relationship of Livin and Smac with menstrual cycle and clinical staging of EMs, as well as correlation analysis.

Methods: 60 cases of patients, who were given laparoscopic surgery or laparotomy operation due to EMs (confirmed by postoperative pathological examinations) in Department of Obstetrics and Gynecology of the Third Affiliated Hospital of Inner Mongolia Medical College from October 2010 to April 2012, were selected and included into the study group. The study group was subdivided into the eutopic group and the ectopic group, each of which contained 30 cases (16 cases for the proliferative phase, 14 cases for the secretory phase). 30 samples of normal endometrial tissues were chosen as the control group. Immunohistochemical method (SP) was used to determine the expression of Livin and Smac proteins in each group, with statistical analysis conducted to the results.

Results: The expression of Livin in eutopic and ectopic endometrial tissues in EMs was significantly higher than that in normal endometrial tissues in the control group, and the difference was statistically significant (χ² = 12.510, p < .05); The expression of Smac in eutopic and ectopic endometrial tissues in EMs was significantly lower than that in normal endometrial tissues in the control group, and the difference was statistically significant (χ² = 19.530, p < .05). The expression of Livin and Smac in the eutopic and the ectopic endometrial tissues in EMs had no correlation to clinical staging (χ² = 0.741 and χ² = 0.002 respectively, all p > .05); In the eutopic and the ectopic endometrial tissues in EMs, the expression of Livin was negatively correlated to the expression of Smac (r_s = -0.933 and r_s = -0.867 respectively, all p < .05).

Conclusions: The high expression of Livin and the low expression of Smac enhance the abilities of hyperplasia and antiapoptosis of ectopic endometrial cells, which leads to the occurrence and development of EMs.