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Effect of Aurora kinase B on polyploidy and decidualization in mouse uterus

Wang, Peng Chao ; Yang, Zhen Shan LU orcid and Gu, Xiao Wei (2023) In American Journal of Reproductive Immunology 90(5).
Abstract

Research question: Decidualization is critical to the establishment of mouse normal pregnancy. The fibroblast-like stromal cells in the process form polyploid multinucleated cells. Aurora kinase B (Aurora B) has previously been shown to regulate polyploidy in various cells. However, whether Aurora B regulates the formation of decidual cell polyploidization and its regulatory mechanisms remain poorly understood. Design:: Establish decidualization model of mouse primary endometrial stromal cells in vitro. Construct pseudopregnancy mouse models and delayed-activation mouse models. Detect Aurora B and polyploidization related genes in mouse uteri treated by Aurora B specific inhibitor Barasertib and CPT. Results:: In this study, we found... (More)

Research question: Decidualization is critical to the establishment of mouse normal pregnancy. The fibroblast-like stromal cells in the process form polyploid multinucleated cells. Aurora kinase B (Aurora B) has previously been shown to regulate polyploidy in various cells. However, whether Aurora B regulates the formation of decidual cell polyploidization and its regulatory mechanisms remain poorly understood. Design:: Establish decidualization model of mouse primary endometrial stromal cells in vitro. Construct pseudopregnancy mouse models and delayed-activation mouse models. Detect Aurora B and polyploidization related genes in mouse uteri treated by Aurora B specific inhibitor Barasertib and CPT. Results:: In this study, we found that Aurora B was strongly expressed in endometrial stromal cells after implantation. Additionally, Aurora B was remarkably up regulated in the stromal cells of oil-induced deciduomoa and in vitro decidualization. As an Aurora B specific inhibitor, Barasertib significantly inhibits the mRNA expression of Prl8a2, a marker of mouse decidualization. Furthermore, the protein levels of p-Plk1, Survivin and p-Cdk1 were inhibited by Barasertib. CPT-induced DNA damage suppressed Aurkb (encodes Aurora B) expression, thus resulting in polyploidization. Conclusion:: Our data shows that Aurora B is expressed in decidual stromal cells of implantation sites and plays a key role for mouse decidualization. The protein of Plk1, Survivn, and Cdk1 may participate in formation of decidual cell polyploidization during mouse decidualization.

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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Aurora B, decidualization, polyploidization, uterus
in
American Journal of Reproductive Immunology
volume
90
issue
5
article number
e13793
publisher
Wiley-Blackwell
external identifiers
  • pmid:37881124
  • scopus:85174828664
ISSN
1046-7408
DOI
10.1111/aji.13793
language
English
LU publication?
yes
id
a6d4118e-f682-4d89-a0d3-1e32182b925a
date added to LUP
2023-12-11 13:34:56
date last changed
2024-04-24 07:02:22
@article{a6d4118e-f682-4d89-a0d3-1e32182b925a,
  abstract     = {{<p>Research question: Decidualization is critical to the establishment of mouse normal pregnancy. The fibroblast-like stromal cells in the process form polyploid multinucleated cells. Aurora kinase B (Aurora B) has previously been shown to regulate polyploidy in various cells. However, whether Aurora B regulates the formation of decidual cell polyploidization and its regulatory mechanisms remain poorly understood. Design:: Establish decidualization model of mouse primary endometrial stromal cells in vitro. Construct pseudopregnancy mouse models and delayed-activation mouse models. Detect Aurora B and polyploidization related genes in mouse uteri treated by Aurora B specific inhibitor Barasertib and CPT. Results:: In this study, we found that Aurora B was strongly expressed in endometrial stromal cells after implantation. Additionally, Aurora B was remarkably up regulated in the stromal cells of oil-induced deciduomoa and in vitro decidualization. As an Aurora B specific inhibitor, Barasertib significantly inhibits the mRNA expression of Prl8a2, a marker of mouse decidualization. Furthermore, the protein levels of p-Plk1, Survivin and p-Cdk1 were inhibited by Barasertib. CPT-induced DNA damage suppressed Aurkb (encodes Aurora B) expression, thus resulting in polyploidization. Conclusion:: Our data shows that Aurora B is expressed in decidual stromal cells of implantation sites and plays a key role for mouse decidualization. The protein of Plk1, Survivn, and Cdk1 may participate in formation of decidual cell polyploidization during mouse decidualization.</p>}},
  author       = {{Wang, Peng Chao and Yang, Zhen Shan and Gu, Xiao Wei}},
  issn         = {{1046-7408}},
  keywords     = {{Aurora B; decidualization; polyploidization; uterus}},
  language     = {{eng}},
  number       = {{5}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{American Journal of Reproductive Immunology}},
  title        = {{Effect of Aurora kinase B on polyploidy and decidualization in mouse uterus}},
  url          = {{http://dx.doi.org/10.1111/aji.13793}},
  doi          = {{10.1111/aji.13793}},
  volume       = {{90}},
  year         = {{2023}},
}