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Promotion of angiogenesis and proliferation cytokines patterns in peritoneal fluid from women with endometriosis.子宫内膜异位症患者腹腔液中血管生成促进因子和增殖细胞因子模式
J Reprod Immunol. 2016 Aug;116:1-6. doi: 10.1016/j.jri.2016.01.005. Epub 2016 Feb 24.
2
Human Endometrial Fibroblasts Derived from Mesenchymal Progenitors Inherit Progesterone Resistance and Acquire an Inflammatory Phenotype in the Endometrial Niche in Endometriosis.源自间充质祖细胞的人子宫内膜成纤维细胞在子宫内膜异位症的子宫内膜微环境中继承孕激素抵抗并获得炎症表型。
Biol Reprod. 2016 May;94(5):118. doi: 10.1095/biolreprod.115.136010. Epub 2016 Apr 13.
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Endometrial stem/progenitor cells: the first 10 years.子宫内膜干细胞/祖细胞:首个十年
Hum Reprod Update. 2016 Mar-Apr;22(2):137-63. doi: 10.1093/humupd/dmv051. Epub 2015 Nov 9.
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CD4+Foxp3+ regulatory T cell differentiation mediated by endometrial stromal cell-derived TECK promotes the growth and invasion of endometriotic lesions.由子宫内膜基质细胞衍生的TECK介导的CD4+Foxp3+调节性T细胞分化促进了子宫内膜异位症病灶的生长和侵袭。
Cell Death Dis. 2014 Oct 2;5(10):e1436. doi: 10.1038/cddis.2014.414.
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Nanoparticle labeling identifies slow cycling human endometrial stromal cells.
Stem Cell Res Ther. 2014 Jul 4;5(4):84. doi: 10.1186/scrt473.
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Potential role of endometrial stem/progenitor cells in the pathogenesis of early-onset endometriosis.子宫内膜干/祖细胞在早发性子宫内膜异位症发病机制中的潜在作用。
Mol Hum Reprod. 2014 Jul;20(7):591-8. doi: 10.1093/molehr/gau025. Epub 2014 Mar 27.
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Endometriosis: pathogenesis and treatment.子宫内膜异位症:发病机制与治疗。
Nat Rev Endocrinol. 2014 May;10(5):261-75. doi: 10.1038/nrendo.2013.255. Epub 2013 Dec 24.
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Possible involvement of signal transducer and activator of transcription-3 in cell-cell interactions of peritoneal macrophages and endometrial stromal cells in human endometriosis.信号转导子和转录激活子 3 可能参与人子宫内膜异位症中腹腔巨噬细胞和子宫内膜基质细胞的细胞间相互作用。
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Endometriosis, a disease of the macrophage.子宫内膜异位症,一种巨噬细胞疾病。
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A subset of human uterine endometrial macrophages is alternatively activated.一部分人类子宫内膜巨噬细胞呈替代性激活状态。
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与巨噬细胞共培养可增强子宫内膜异位症基质细胞的克隆形成和侵袭活性。

Co-culture with macrophages enhances the clonogenic and invasion activity of endometriotic stromal cells.

作者信息

Chan Rachel W S, Lee Cheuk-Lun, Ng Ernest H Y, Yeung William S B

机构信息

Department of Obstetrics and Gynaecology, The University of Hong Kong, Hong Kong, China.

Centre of Reproduction, Development of Growth, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, China.

出版信息

Cell Prolif. 2017 Jun;50(3). doi: 10.1111/cpr.12330. Epub 2017 Jan 10.

DOI:10.1111/cpr.12330
PMID:28071833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6529078/
Abstract

OBJECTIVE

To study the effect on endometrial and endometriotic cells after co-culture with macrophages, using clonogenic, invasion and self-renewal assays.

MATERIALS AND METHODS

Peripheral blood samples, endometrium and endometriotic tissues were collected. Autologous macrophages were co-cultured with endometrial and endometriotic cells. The number of colony-forming units (CFU), invasiveness and self-renewal activity after co-culture with macrophages were determined. The cytokine level of colony-stimulating factor-1 (CSF-1) from macrophages with and without endometriosis was compared.

RESULTS

Co-culture with macrophages significantly increased the clonogenic and invasion ability of endometriotic stromal cells in vitro. Colony-stimulating factor-1 (CSF-1) was up-regulated in endometriotic macrophages conditioned medium when compared to those without the disease.

CONCLUSIONS

These data suggest that macrophages may increase the proliferation and invasion activity of stromal clonogenic cells in women with endometriosis.

摘要

目的

采用克隆形成、侵袭和自我更新分析方法,研究巨噬细胞与子宫内膜细胞和子宫内膜异位症细胞共培养后的影响。

材料与方法

采集外周血样本、子宫内膜和子宫内膜异位症组织。将自体巨噬细胞与子宫内膜细胞和子宫内膜异位症细胞共培养。测定与巨噬细胞共培养后的集落形成单位(CFU)数量、侵袭性和自我更新活性。比较有和没有子宫内膜异位症的巨噬细胞的集落刺激因子-1(CSF-1)细胞因子水平。

结果

与巨噬细胞共培养显著提高了子宫内膜异位症基质细胞在体外的克隆形成和侵袭能力。与无该疾病的巨噬细胞相比,子宫内膜异位症巨噬细胞条件培养基中的集落刺激因子-1(CSF-1)上调。

结论

这些数据表明,巨噬细胞可能会增加子宫内膜异位症女性基质克隆形成细胞的增殖和侵袭活性。