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Expression of chemokine CXCL14 in the proliferative-phase endometriosis |
ZOU Ruanmin1, LIN Kezhi2, YU Xia3, YU Jianqin1, RUAN Jingyao3, CHEN Guan’ge1, ZHANG Wenmiao1. |
1.Department of Obstetrics and Gynecology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015; 2.Medical Experimental Teaching Center, Wenzhou Medical University, Wenzhou, 325035; 3.Department of Pathology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015
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Cite this article: |
ZOU Ruanmin,LIN Kezhi,YU Xia, et al. Expression of chemokine CXCL14 in the proliferative-phase endometriosis[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2016, 46(6): 422-426.
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Abstract Objective: To analyze the expression of chemokine CXCL14 in the eutopic and ectopic endometrium of the proliferative-phase endometriosis. Methods: Real-time PCR and immunohistochemistry were adopted to measure and compare the CXCL14 expression in 18 cases of eutopic endometrium, 24 cases of ectopic endometrium and 20 cases of normal endometrium, which were confirmed by surgery and pathology. Results: ①Compared to normal endometrium, the expression of chemokine CXCL14 at mRNA and protein levels significantly declined in eutopic endometrium with stage III-IV, there were significant differences (P<0.05). ②Compared to normal endometrium, the expression of chemokine CXCL14 at mRNA and protein levels declined slightly in eutopic endometrium with stage I-II, but there were no significant differences. ③The chemokine CXCL14 at mRNA and protein levels were significantly down-regulated in ectopic endometrium with stage III-IV compared to eutopic endometrium with stage III-IV (P<0.05). ④The chemokine CXCL14 at mRNA and protein levels were slightly down-regulated in ectopic endometrium with stage I-II compared to eutopic endometrium with stage I-II. Conclusion: Our findings indicated that CXCL14 may participate in the development and progression of endometriosis, which is likely associated with the low conception rates in women with endometriosis.
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Received: 20 January 2016
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