生物
细胞生物学
子宫
干细胞
造血
炎症
内科学
作者
Juan Liu,Yanyun Ying,Siwen Wang,Jing-Yi Li,Jinqun Xu,Ping-Ping Lv,Jianhua Chen,Caiyun Zhou,Yifeng Liu,Yiqing Wu,Yun Huang,Yao Chen,Lifen Chen,Shijiong Tu,Wei Zhao,Min Yang,Yanjun Hu,Run-Ju Zhang,Dan Zhang
出处
期刊:Cytokine
[Elsevier]
日期:2020-01-01
卷期号:125: 154850-154850
被引量:3
标识
DOI:10.1016/j.cyto.2019.154850
摘要
Abstract Background Endometrial injury can result in thin endometrium and subfertility. Granulocyte macrophage colony stimulating factor (GM-CSF) contributes to tissue repair, but its role in endometrial regeneration has not been investigated. Methods To determine the effect of GM-CSF on endometrial regeneration, we established a mouse model of thin endometrium by uterine perfusion with 20 μL 90% ethanol. Thin endometrium in mice was featured by lowered endometrial thickness, decreased expression of Ki67 in glandular cells, and a reduced number of implantation sites. To explore the mechanism of GM-CSF on endometrial regeneration, endometrium was obtained from patients undergoing hysterectomy or hysteroscopy and endometrial biopsy. Effects of GM-CSF on primary cultured human endometrial glandular and stromal cells were examined by the 5-bromo-2′-deoxyuridine (BrdU) proliferation assay and transwell migration assay, followed by exploration of the potential signaling pathway. Results GM-CSF intraperitoneal (i.p.) injection significantly increased endometrial thickness, expression of Ki67 in endometrial glandular cells, and the number of implantation sites. GM-CSF significantly promoted proliferation of primary human endometrial glandular cells and migration of stromal cells. GM-CSF activated p-Akt and increased expressions of p70S6K and c-Jun, which were blocked by LY294002. Conclusion We found that GM-CSF could improve endometrial regeneration, possibly through activating PI3K/Akt signaling pathway.
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