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A Potential Role of CD82/KAI1 during Uterine Decidualization in Mice.
Li, Qijun; Song, Mengyao; Cao, Ke; Zhang, Qian.
Affiliation
  • Li Q; Laboratory Animal Center, Chongqing Medical University, Chongqing 400016, China.
  • Song M; Laboratory Animal Center, Chongqing Medical University, Chongqing 400016, China.
  • Cao K; Laboratory Animal Center, Chongqing Medical University, Chongqing 400016, China.
  • Zhang Q; Laboratory Animal Center, Chongqing Medical University, Chongqing 400016, China.
Curr Issues Mol Biol ; 46(3): 1799-1809, 2024 Feb 27.
Article in En | MEDLINE | ID: mdl-38534734
ABSTRACT
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.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Curr Issues Mol Biol Year: 2024 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Curr Issues Mol Biol Year: 2024 Document type: Article