An IGF1-expressing endometrial stromal cell population is associated with human decidualization.
An IGF1-expressing endometrial stromal cell population is associated with human decidualization.
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表达 IGF1 的子宫内膜基质细胞群与人类蜕膜化相关
DOI：
10.1186/s12915-022-01483-0
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发表时间：
2022-12-08
期刊：
影响因子：
5.4
通讯作者：
Li, Ming-Qing
中科院分区：
文献类型：
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作者：
Shi, Jia-Wei;Lai, Zhen-Zhen;Yang, Hui-Li;Zhou, Wen-Jie;Zhao, Xiao-Ya;Xie, Feng;Liu, Song-Ping;Chen, Wei-Dong;Zhang, Tao;Ye, Jiang-Feng;Zhou, Xiang-Yu;Li, Ming-Qing
蜕质化是指子宫内膜间质成纤维细胞转化为特化的蜕质细胞的过程，蜕质细胞为囊胚着床和胎盘发育提供了必需的营养和免疫基质。脱个体化缺陷与多种妊娠疾病有关，包括女性不孕症、复发性植入失败（RIF）和流产。尽管越来越多的基因被报道与子宫内膜容受性和脱个体化相关，但触发和潜在的脱个体化的细胞和分子机制仍然很大程度上未知。在这里，我们分析了着床期子宫内膜细胞和妊娠早期蜕膜细胞的单细胞转录谱，以获得对蜕膜过程的见解。结果通过单细胞RNA测序，我们观察到一种独特的IGF1+基质细胞可能启动去个体化。我们发现IL1B+基质细胞促进腺体变性和蜕膜止血。我们定义了一个NK细胞亚群，通过AREG-IGF1和AREG-CSF1调控轴加速脱细胞化和外滋养细胞（EVT）侵袭。进一步分析表明EVT可能通过多种途径促进去个体化。此外，还开发了一个系统的细胞-细胞通信库，用于去个体化。在不明原因的RIF患者中观察到IGF1+基质细胞向IGF1R+基质细胞的异常转换比例。总之，IGF1+基质细胞的一个独特亚群参与了去个体化的启动。我们的观察结果为脱个体化的分子和细胞特征提供了更深入的见解，并为进一步发展脱个体化程度的评估和脱个体化障碍相关疾病的治疗提供了平台。
BackgroundDecidualization refers to the process of transformation of endometrial stromal fibroblast cells into specialized decidual stromal cells that provide a nutritive and immunoprivileged matrix essential for blastocyst implantation and placental development. Deficiencies in decidualization are associated with a variety of pregnancy disorders, including female infertility, recurrent implantation failure (RIF), and miscarriages. Despite the increasing number of genes reportedly associated with endometrial receptivity and decidualization, the cellular and molecular mechanisms triggering and underlying decidualization remain largely unknown. Here, we analyze single-cell transcriptional profiles of endometrial cells during the window of implantation and decidual cells of early pregnancy, to gains insights on the process of decidualization.ResultsWe observed a unique IGF1+stromal cell that may initiate decidualization by single-cell RNA sequencing. We found the IL1B+stromal cells promote gland degeneration and decidua hemostasis. We defined a subset of NK cells for accelerating decidualization and extravillous trophoblast (EVT) invasion by AREG-IGF1 and AREG-CSF1 regulatory axe. Further analysis indicates that EVT promote decidualization possibly by multiply pathways. Additionally, a systematic repository of cell–cell communication for decidualization was developed. An aberrant ratio conversion of IGF1+stromal cells to IGF1R+stromal cells is observed in unexplained RIF patients.ConclusionsOverall, a unique subpopulation of IGF1+stromal cell is involved in initiating decidualization. Our observations provide deeper insights into the molecular and cellular characterizations of decidualization, and a platform for further development of evaluation of decidualization degree and treatment for decidualization disorder-related diseases.
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影响因子：
82.9
作者：
Cha J;Sun X;Dey SK
通讯作者：
Dey SK
影响因子：
6.7
作者：
Laufer, Neri;Simon, Alex
通讯作者：
Simon, Alex
影响因子：
4
作者：
Chen, Wenqi;Lu, Siyu;Gao, Rufei
通讯作者：
Gao, Rufei
影响因子：
6.7
作者：
Garrido-Gomez, Tamara;Ruiz-Alonso, Maria;Simon, Carlos
通讯作者：
Simon, Carlos
DOI：
10.1111/aji.12473
发表时间：
2016-03
期刊：
American journal of reproductive immunology (New York, N.Y. : 1989)
影响因子：
--
作者：
Bhurke AS;Bagchi IC;Bagchi MK
通讯作者：
Bagchi MK