A positive COX-2/IL-1β loop promotes decidualization by upregulating CD82

Qu, Qiuchan; Shen, Hui‐Hui; Wang, Chengjie; Zhang, Xinyan; Wu, Jiang‐Nan; Lu, Hang-Cheng; Ding, Jian; Tan, Xiaofang; Liu, Libing; Li, Ming‐Qing

doi:10.1530/rep-21-0204

Cited by 6 publications

(3 citation statements)

References 49 publications

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“…Our observations reveal that CD82/KAI1 participated in the process of stromal cell decidualization. Parallel findings by Qu et al [ 24 ] in human tissues suggest that CD82/KAI1 could serve as a novel promoter for decidualization within a positive feedback loop. In other words, CD82/KAI1 is found in stromal cells when decidualization is induced artificially using oil, revealing that the expression of CD82/KAI1 is not straightforwardly dependent on the implantation of blastocysts.…”

Section: Discussionsupporting

confidence: 70%

A Potential Role of CD82/KAI1 during Uterine Decidualization in Mice

Li,

Song,

Cao

et al. 2024

CIMB

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The tumor metastasis suppressor gene CD82/KAI1 has been demonstrated to impact human trophoblast invasion and migration. Communication between trophoblasts and decidual stromal cells plays a crucial role in controlling the normal invasiveness of trophoblasts. However, whether CD82/KAI1 is involved in decidualization and what role it plays remain unclear. CD82/KAI1 demonstrates specific spatiotemporal expression patterns in stromal cells undergoing decidualization during pregnancy. This is observed in both naturally pregnant females post-implantation and pseudopregnant mice undergoing induced decidualization, as detected through in situ hybridization and immunofluorescence. CD82/KAI1 expression showed a significant time-dependent increase in cultured stromal cells after 24 and 48 h of progesterone (P4) and estrogen (E2) treatment. This was accompanied by a notable upregulation of decidualization markers, including cyclin D3 and PR. After transducing stromal cells with the adenovirus-overexpressing CD82/KAI1 for 48 h, the expression of cyclin D3 protein increased. Meanwhile, there was an attenuated expression of CD82/KAI1 due to an adenovirus siRNA knockdown, whereas cyclin D3 and PR expressions were not affected. Our findings suggest a potential role of CD82/KAI1 in regulating the process of decidualization, providing insights into stromal cell differentiation.

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Section: Discussionsupporting

confidence: 70%

A Potential Role of CD82/KAI1 during Uterine Decidualization in Mice

Li,

Song,

Cao

et al. 2024

CIMB

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“…This observation deepens our understanding of the mechanism of epithelial cell degeneration in the process of endometrial decidualization. In view of the important role of IL1B in decidualization [57], the role of theIL1B + dSec-SC in the development of decidualization cannot be ignored yet.…”

Section: Discussionmentioning

confidence: 99%

An IGF1-expressing endometrial stromal cell population is associated with human decidualization

et al. 2022

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Background Decidualization 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. Results We 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. Conclusions Overall, 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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“…Folate has also been shown to attenuate LPS-induced increases in COX-2 in mouse placentae [163]. As COX-2 plays a positive role in decidualization [164,165], FRα signaling may be a regulator that balances COX-2 for optimal status during pregnancy. Notably, certain crucial genes associated with the cellular cycle (Trp53), differentiation (Nr1h3, Nr5a1), and angiogenesis (Ereg), were hypermethylated and therefore downregulated in the decidua [92].…”

Section: Decidualizationmentioning

confidence: 99%

Recent Advances in Folates and Autoantibodies against Folate Receptors in Early Pregnancy and Miscarriage

Qin,

Ha,

Chen

et al. 2023

Nutrients

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Though firstly identified in cerebral folate deficiency, autoantibodies against folate receptors (FRAbs) have been implicated in pregnancy complications such as miscarriage; however, the underlying mechanism needs to be further elaborated. FRAbs can be produced via sensitization mediated by folate-binding protein as well as gene mutation, aberrant modulation, or degradation of folate receptors (FRs). FRAbs may interfere with folate internalization and metabolism through blocking or binding with FRs. Interestingly, different types of FRs are expressed on trophoblast cells, decidual epithelium or stroma, and macrophages at the maternal-fetal interface, implying FRAbs may be involved in the critical events necessary for a successful pregnancy. Thus, we propose that FRAbs may disturb pregnancy establishment and maintenance by modulating trophoblastic biofunctions, placental development, decidualization, and decidua homeostasis as well as the functions of FOLR2+ macrophages. In light of these findings, FRAbs may be a critical factor in pathological pregnancy, and deserve careful consideration in therapies involving folic acid supplementation for pregnancy complications.

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A positive COX-2/IL-1β loop promotes decidualization by upregulating CD82

Cited by 6 publications

References 49 publications

A Potential Role of CD82/KAI1 during Uterine Decidualization in Mice

A Potential Role of CD82/KAI1 during Uterine Decidualization in Mice

An IGF1-expressing endometrial stromal cell population is associated with human decidualization

Recent Advances in Folates and Autoantibodies against Folate Receptors in Early Pregnancy and Miscarriage

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