Expression of Bcl-2, Smac and their correlation in endometriosis

Ping Zhu, Shuna Shen
In: Discussion of Clinical Cases · 2017 · vol. 4(4) , pp. 11 · doi:10.14725/dcc.v4n4p11 · W2794860235
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Endometriosis tissues showed significantly higher Bcl-2 and lower Smac expression compared to normal endometrium, suggesting these altered levels contribute to the disease's development.

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This study investigated the expression levels of the anti-apoptotic protein Bcl-2 and the pro-apoptotic protein Smac in endometrial tissues from patients with endometriosis compared to normal controls. Using immunohistochemistry on samples from both proliferative and secretory phases, researchers found that Bcl-2 expression was significantly higher while Smac expression was significantly lower in both eutopic and ectopic endometrial tissues of endometriosis patients. The analysis revealed a negative correlation between Bcl-2 and Smac levels, indicating that this imbalance enhances cell hyperplasia and anti-apoptotic capabilities in ectopic tissue. These molecular changes were not associated with clinical staging but are proposed as mechanisms driving the occurrence and development of the disease. This paper is centrally about endometriosis — specifically examining the molecular pathways involving apoptosis regulation in ectopic endometrial lesions.

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Abstract

Objective: To explore the expression of anti-apoptotic gene Bcl-2 and second mitochondria-derived activator of caspases (Smac) in endometriosis, the relationship of Bcl-2 and Smac with clinical staging and menstrual cycle, as well as correlation analysis. Methods: Thirty samples of endometrial tissues taken from endometriosis patients were chosen as the study group (endometriosis group), including 16 cases in the proliferative phase and 14 cases in the secretory phase. Thirty samples of normal endometrial tissues were chosen as the control group. Immunohistochemical method (SP) was used to determine the expression of Bcl-2 and Smac proteins in each group. Statistical analysis was carried out with SPSS 16.0 statistical package. The comparison of measurement data between two groups was made by use of chi-square (χ 2 ) test, and the correlation test of two indexes was performed by use of Spearman’s correlation analysis. The difference in statistical data was of statistical significance ( p < .05). Results: The expression of Bcl-2 in eutopic and ectopic endometrial tissues in the endometriosis group was significantly higher than that in normal endometrial tissues in the control group, and the difference was statistically significant ( p < .05). The difference of Bcl-2 expression in all phases of both eutopic tissues in the endometriosis group and normal endometrial tissues was statistically significant ( p < .05), the positive expression in the secretory phase was obviously lower than that in the proliferative phase. The expression intensity of Smac in eutopic and ectopic endometrial tissues in the endometriosis group was lower than that in normal endometrial tissues in the control group, and the difference was of statistical significance ( p < .05). The expression intensity of Smac in ectopic endometrial tissues was lower than that in eutopic endometrial tissues, and the difference was of statistical significance ( p < .05); the expression intensity of Smac in the secretory phase was higher than that in the proliferative phase in normal endometrial tissues ( p .05). The expression of Bcl-2 was negatively correlated to the expression of Smac ( p < .05). Conclusions: The high expression of Bcl-2 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 endometriosis.
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Abstract

Objective: To explore the expression of anti-apoptotic gene Bcl-2 and second mitochondria-derived activator of caspases (Smac) in endometriosis, the relationship of Bcl-2 and Smac with clinical staging and menstrual cycle, as well as correlation analysis.

Methods

Thirty samples of endometrial tissues taken from endometriosis patients were chosen as the study group (endometriosis group), including 16 cases in the proliferative phase and 14 cases in the secretory phase. Thirty samples of normal endometrial tissues were chosen as the control group. Immunohistochemical method (SP) was used to determine the expression of Bcl-2 and Smac proteins in each group. Statistical analysis was carried out with SPSS 16.0 statistical package. The comparison of measurement data between two groups was made by use of chi-square (χ2) test, and the correlation test of two indexes was performed by use of Spearman’s correlation analysis. The difference in statistical data was of statistical significance (p < .05).

Results

The expression of Bcl-2 in eutopic and ectopic endometrial tissues in the endometriosis group was significantly higher than that in normal endometrial tissues in the control group, and the difference was statistically significant (p < .05). The difference of Bcl-2 expression in all phases of both eutopic tissues in the endometriosis group and normal endometrial tissues was statistically significant (p < .05), the positive expression in the secretory phase was obviously lower than that in the proliferative phase. The expression intensity of Smac in eutopic and ectopic endometrial tissues in the endometriosis group was lower than that in normal endometrial tissues in the control group, and the difference was of statistical significance (p < .05). The expression intensity of Smac in ectopic endometrial tissues was lower than that in eutopic endometrial tissues, and the difference was of statistical significance (p < .05); the expression intensity of Smac in the secretory phase was higher than that in the proliferative phase in normal endometrial tissues (p .05). The expression of Bcl-2 was negatively correlated to the expression of Smac (p < .05).

Conclusions

The high expression of Bcl-2 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 endometriosis. Full Text: PDFDOI: https://doi.org/10.5430/dcc.v4n4p11 Refbacks - There are currently no refbacks.

Discussion

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endometriosis

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