Ovarian expression of MerTK and its ligand Pros1 in non-pregnant estrus and pregnant mice.

Aim: The interaction of MerTK, which negatively regulates immune responses, with its ligand Pros1 contributes to the resolution of apoptosis and inflammation, participating in the healing process of tissues. The levels of MerTK and Pros1, intensely expressed in macrophages (Mϕs), are affected by sex hormones. The expression levels of these proteins in Mϕs, which have a role in corpus luteum (CL) development or regression and folliculogenesis, were investigated in this study since their expressions have not been evaluated in pregnant mouse ovaries.
Method: We analyzed mouse ovaries from non-pregnant mice at estrus and gestation days 5, 8, and 15 (each n:10). We used qPCR to evaluate Mertk and Pros1 mRNA levels and assessed their protein expression and localization using immunohistochemistry and double immunofluorescence staining for co-localization.
Results: Mertk and Pros1 mRNA and protein levels significantly increased in GD15. MerTK and Pros1 protein levels in mouse CL on GD15 were significantly higher than all other groups. MerTK and Pros1 positive Mϕs were observed in CL of GD15 by double immunofluorescence. MerTK protein levels were increased in granulosa cells GD15 of primary and growing follicles.
Conclusion: Our study revealed for the first time that the expression of MerTK and Pros1 was significantly increased in CL at GD15 in mice. These results suggest that increased levels of MerTK andPros1 may enhance their interaction as receptor-ligand binding partners in CL potentially contributing to the balance of apoptosis and inflammation.
Competing Interests: Declarations. Institutional review board statement: The Animal Research Ethics Local Committee, Akdeniz University, approved the research by B.30.2.AKD.0.05.07.00/2 number. The Akdeniz University Institutional Animal Care and Use Committee standards carried out all experimental protocols on mice. Conflict of interest: The authors report no declarations of interest.
(© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)