Liqin Ji1, Liping Zhang2, Yani Li3, Li Guo1, Ni Cao4, Zhiying Bai5, Yingchun Song6, Zhao Xu4, Juan Zhang7, Chunhua Liu8, Xiaoxing Ma9. 1. Obstetrical Department, No.215 Hospital of Shanxi Nuclear Industry, Xianyang, Shaanxi, 712000, China. 2. Obstetrical Department, Yan'an University Affiliated Hospital, Yan'an, Shaanxi, 716000, China. 3. The 2nd Department of Obstetrical, Northwest Women and Children's Hospital, Xian, Shaanxi, 710000, China. 4. Obstetrical Department, Northwest Women and Children's Hospital, Xian, Shaanxi, 710000, China. 5. Gynaecology and Obstetrics, 4th (Xing Yuan) Hospital of Yulin, Yulin, Shaanxi, 719000, China. 6. Gynaecology and Obstetrics, Xian NO.1 Hospital, Xian, Shaanxi, 710000, China. 7. Obstetrical Department, Yan'an University Affiliated Hospital, Yan'an, Shaanxi, 716000, China. Electronic address: zhangjuan19720803@163.com. 8. Obstetrical Department, Shaanxi Baoji Maternal and Child Health Hospital, Baoji 721000, China. Electronic address: liuchunhua1967@126.com. 9. Obstetrical Department, Yan'an People's Hospital, Yanan, Shaanxi, 716000, China. Electronic address: maxiaoxing04@163.com.
Abstract
INTRODUCTION: Mesenchymal stem cells (MSCs) play an important role in the pathology of preeclampsia (PE). The survival of MSCs and angiogenesis in the maternal-fetal interface are important for a successful pregnancy. MicroRNA-136 (miR-136) is highly expressed in decidua-derived MSCs (MSCs) from PE compared with healthy donors (NC). The role of the MSCs aberrant expressed miR-136 in PE development is still unclear. In the present study, we examined the impact of miR-136 on the survival of MSCs and angiogenesis in the maternal-fetal interface. METHODS: MSCs were extracted and transfected with miR-136 mimic and interfering RNAs using lipofectamine-2000. Then cell apoptosis were tested using flow cytometry. HUVEC tube formation ability was tested on Matrigel co-cultured with conditioned MSCs supernatants. RESULTS: High level of miR-136 could suppress cell proliferation and promote apoptosis of MSCs through targeting BCL2. It could also impairs HUVEC capillary formation by suppressing VEGF. DISCUSSION: MiR-136 significantly increase the apoptosis and suppress the proliferation of MSCs. It could also inhibit the capillary formation and trophoblast cell invasion. These data suggest that decidua-derived miR-136 that is increased in PE is a potential causal factor of PE.
INTRODUCTION: Mesenchymal stem cells (MSCs) play an important role in the pathology of preeclampsia (PE). The survival of MSCs and angiogenesis in the maternal-fetal interface are important for a successful pregnancy. MicroRNA-136 (miR-136) is highly expressed in decidua-derived MSCs (MSCs) from PE compared with healthy donors (NC). The role of the MSCs aberrant expressed miR-136 in PE development is still unclear. In the present study, we examined the impact of miR-136 on the survival of MSCs and angiogenesis in the maternal-fetal interface. METHODS: MSCs were extracted and transfected with miR-136 mimic and interfering RNAs using lipofectamine-2000. Then cell apoptosis were tested using flow cytometry. HUVEC tube formation ability was tested on Matrigel co-cultured with conditioned MSCs supernatants. RESULTS: High level of miR-136 could suppress cell proliferation and promote apoptosis of MSCs through targeting BCL2. It could also impairs HUVEC capillary formation by suppressing VEGF. DISCUSSION: MiR-136 significantly increase the apoptosis and suppress the proliferation of MSCs. It could also inhibit the capillary formation and trophoblast cell invasion. These data suggest that decidua-derived miR-136 that is increased in PE is a potential causal factor of PE.
Authors: Gary P Brennan; Dimitrios M Vitsios; Sophie Casey; Ann-Marie Looney; Boubou Hallberg; David C Henshall; Geraldine B Boylan; Deirdre M Murray; Catherine Mooney Journal: PLoS One Date: 2018-12-03 Impact factor: 3.240