›› 2013, Vol. 33 ›› Issue (3): 269-.doi: 10.3969/j.issn.1674-8115.2013.03.003

• 论著(基础研究) • 上一篇    下一篇

Activin A与子宫内膜异位症的相关性研究

苏小玲, 赵爱民, 施 君, 祝 捷, 季 芳, 楼微华   

  1. 上海交通大学 医学院附属仁济医院妇产科, 上海 200127
  • 出版日期:2013-03-28 发布日期:2013-03-29
  • 通讯作者: 赵爱民, 电子信箱: zamzkh0526@126.com。
  • 作者简介:苏小玲(1986—), 女, 硕士生; 电子信箱: sxl292009@126.com。
  • 基金资助:

    上海市科委重大项目 (11140903601)

Relationship between Activin A and endometriosis

SU Xiao-ling, ZHAO Ai-min, SHI Jun, ZHU Jie, JI Fang, LOU Wei-hua   

  1. Department of Obstetrics and Gynaecology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200127, China
  • Online:2013-03-28 Published:2013-03-29
  • Supported by:

    Shanghai Science and Technology Committee Foundation, 11140903601

摘要:

目的 探讨Activin A对子宫内膜细胞迁移、侵袭、增殖、黏附的影响及其机制。方法 无菌收集正常分泌期子宫内膜,分离、培养内膜原代细胞,以0(对照)、8、16、32、64 ng/mL Activin A孵育内膜腺上皮细胞、间质细胞12 h。采用体外细胞划痕实验、Transwell侵袭实验探讨不同浓度Activin A对子宫内膜间质细胞、腺上皮细胞迁移、侵袭的影响;采用CCK8法检测16 ng/mL Activin A对子宫内膜间质细胞、腺上皮细胞增殖、黏附的影响;采用Real-Time PCR检测16 ng/mL Activin A作用下子宫内膜间质细胞、腺上皮细胞血管内皮生长因子A (VEGFA)、VEGF-C mRNA表达变化。结果 体外细胞划痕实验结果显示,不同浓度Activin A处理组子宫内膜细胞划痕14 h前后面积差与对照组比较,差异无统计学意义(P>0.05)。Transwell侵袭实验结果显示:8、16、32 ng/mL Activin A处理组子宫内膜间质细胞穿透细胞数量较对照组明显增多(P<0.05);16、32 ng/mL Activin A处理组腺上皮细胞穿透细胞数量较对照组明显增多(P<0.05);16 ng/mL Activin A处理组穿透细胞数量最多。经16 ng/mL Activin A处理的子宫内膜细胞增殖、黏附能力与对照细胞比较,差异无统计学意义(P>0.05)。经16 ng/mL Activin A处理的子宫内膜间质细胞和腺上皮细胞内VEGF-A、VEGF-C mRNA的表达与对照细胞比较,差异无统计学意义(P>0.05)。结论 Activin A可显著增强子宫内膜细胞的侵袭力,而对细胞迁移、增殖和黏附能力无明显影响;Activin A并非通过调节内膜细胞VEGF-A、VEGF-C的表达而使内膜细胞的侵袭力增强。

关键词: Activin A, 子宫内膜异位症, 侵袭, 血管内皮生长因子

Abstract:

Objective To investigate the effects of Activin A on the invasiveness, migration, adhesion and proliferation of endometrial cells, and explore the mechanism. Methods The endometrium in secretion phase was collected, primary endometrial cells were isolated and cultured, and endometrial stromal cells and endometrial epithelial cells were incubated with 0 ng/mL (control), 8 ng/mL, 16 ng/mL, 32 ng/mL and 64 ng/mL Activin A for 12 h. The effects of different concentrations of Activin A on the migration and invasiveness of endometrial stromal cells and endometrial epithelial cells were determined by in vitro scratch test and Transwell invasion test, the effects of 16 ng/mL Activin A on the proliferation and adhesion of endometrial stromal cells and endometrial epithelial cells were measured by CCK8 method, and the effects of 16 ng/mL Activin A on the expression of vascular endothelial growth factor A (VEGF-A) mRNA and VEGF-C mRNA in endometrial stromal cells and endometrial epithelial cells were detected by Real-Time PCR. Results In vitro scratch test revealed that the differences in areas of scratch of endometrial cells within 14 h in different concentrations Activin A groups were not significantly different from that in control group (P>0.05). Transwell invasion test indicated that the numbers of penetrating cells among endometrial stromal cells in 8 ng/mL, 16 ng/mL and 32 ng/mL Activin A treatment groups were significantly larger than that in control group (P<0.05), the numbers of penetrating cells among endometrial epithelial cells in 16 ng/mL and 32 ng/mL Activin A treatment groups were significantly larger than that in control group (P<0.05), and the number of penetrating cells was the largest in 16 ng/mL Activin A treatment group. The proliferation and adhesion of endometrial cells treated with 16 ng/mL Activin A were not significantly different from those of controls (P>0.05). The expression of VEGF-A mRNA and VEGF-C mRNA in endometrial stromal cells and endometrial epithelial cells treated with 16 ng/mL Activin A was not significantly different from that in controls (P>0.05). Conclusion Activin A can significantly increase the invasiveness of endometrial cells, while has no significant effect on the migration, proliferation and adhesion of endometrial cells. The increase of invasiveness of endometrial cells regulated by Activin A is not related to the regulation of expression of VEGF-A and VEGF-C in endometrial cells.

Key words: Activin A, endometriosis, invasion, vascular endothelial growth factor