Results
The positive rates of PDCD5 protein in ectopic endometrium, eutopic endometrium, and normal endometrium were 30%, 29%, and 75%, respectively. The expression of PDCD5 protein in ectopic endopmetrium and eutopic endometrium was both significantly lower than that in normal endometrium (P=0.004 and 0.007, respectively). There was no significant difference in the expression of PDCD5 protein between ectopic endometrium and eutopic endometrium (P=0.928). The relative expression of PDCD5 mRNA in ectopic endometrium, eutopic endometrium, and normal endometrium was 0.24±0.02, 0.27±0.03, and 1.00±0.04, respectively. The expression of PDCD5 mRNA in ectopic endometrium and eutopic endometrium was both significantly lower than that in normal endometrium (t=-32.098, P<0.001; t=-28.659, P<0.001). There was no significant difference in the expression of PDCD5 mRNA between eutopic endometrium and ectopic endometrium (t=-1.617, P=0.181). The trend of mRNA expression is consistent with that of protein expression. Knockdown of PDCD5 had no significant effect on the morphology and proliferation of ectopic endometrial stromal cells in vitro. CCK-8 assay showed that with the increase of leuprorelin concentration, the proliferation inhibition rate of cells in the PDCD5 knock-down group and control group increased gradually, and at the same concentration of leuprorelin, the cell proliferation inhibition rate was significantly lower in the PDCD5 knockdown group than in the control group (P<0.05). TUNEL assay showed that the apoptosis rate of cells treated with leuprorelin at 0.1 μg/ml was significantly in the PDCD5 knockdown group (0.06±0.01) than in the control group (0.13±0.02) (t=-5.972, P<0.001).
Conclusion
PDCD5 knockdown can reduce the sensitivity of ectopic endometrial stromal cells to leuprorelin, resulting in decreased apoptosis and increased cell proliferation. The down-regulation of PDCD5 expression in ovarian endometriosis may promote the occurrence and development of endometriosis.
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