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从一名子宫发育不全患者的残角子宫中分离出共表达胚胎干细胞和间充质干细胞标志物的细胞群体。

Isolation of a Population of Cells Co-Expressing Markers of Embryonic Stem Cells and Mesenchymal Stem Cells from the Rudimentary Uterine Horn of a Patient with Uterine Aplasia.

作者信息

Burunova V V, Gisina A M, Yarygina N K, Sukhinich K K, Makiyan Z N, Yarygin K N

机构信息

V. N. Orekhovich Research Institute of Biomedical Chemistry, Moscow, Russia.

LLC " NPC Stemma", Moscow, Russia.

出版信息

Bull Exp Biol Med. 2023 Feb;174(4):549-555. doi: 10.1007/s10517-023-05746-w. Epub 2023 Mar 10.

DOI:10.1007/s10517-023-05746-w
PMID:36894816
Abstract

More than 50% cells isolated from the endometrial cavity scraping and the myometrium of the rudimentary horn of an underdeveloped uterus removed from a patient with uterine aplasia and maintained under culturing conditions normal for mesenchymal stem cells (MSC) expressed embryonic transcription factors Oct4 and Nanog, embryonic cell membrane sialyl glycolipid SSEA4, and MSC markers. After 2-3 passages, the cells lost the expression of the early embryogenesis markers, but retained MSC markers. The presence of dormant stem cells in the underdeveloped endometrium and in the uterus indicates that this tissue has a regenerative potential that can be activated and used for completion of organ morphogenesis. This task requires the development of methods of early diagnosis of morphogenesis impairment and tools for safe reactivation of the ontogenesis.

摘要

从子宫发育不全患者切除的未发育子宫残角的子宫内膜腔刮片和子宫肌层中分离出的细胞,超过50%在间充质干细胞(MSC)正常培养条件下培养时表达胚胎转录因子Oct4和Nanog、胚胎细胞膜唾液酸糖脂SSEA4以及MSC标志物。传代2 - 3次后,细胞失去早期胚胎发生标志物的表达,但保留了MSC标志物。未发育的子宫内膜和子宫中存在休眠干细胞,这表明该组织具有再生潜力,可被激活并用于完成器官形态发生。这项任务需要开发形态发生损伤的早期诊断方法以及安全重新激活个体发育的工具。

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Stem Cells Transl Med. 2022 Mar 3;11(1):2-13. doi: 10.1093/stcltm/szab005.
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Stem Cell Res Ther. 2022 Feb 5;13(1):60. doi: 10.1186/s13287-022-02703-8.
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Human Uterine Rudiments: Histological and Immunohistochemical Study.
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Postnatal Pluripotent Cells: Quarter of a Century of Research.产后多能细胞:二十五载研究路。
Bull Exp Biol Med. 2021 Feb;170(4):515-521. doi: 10.1007/s10517-021-05099-2. Epub 2021 Mar 13.
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