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Updated: Jun 8, 2025
Isolation of Mouse Endometrial Epithelial and Stromal Cells for In Vitro Decidualization
Published on: March 2, 2017
Molybdenum interferes with MMPs/TIMPs expression to reduce the receptivity of porcine endometrial epithelial cells
Xiao-Ying Gao1, Yan Zhang1, Wen-Peng Zhao1
1Henan Key Laboratory of Environmental and Animal Product Safety, College of Animal Science and Technology, Henan University of Science and Technology, Kaiyuan Avenue 263, Luoyang, 471000, Henan, PR China.
Abstract:
To investigate the effect of trace element molybdenum (Mo) on the receptivity of porcine endometrial epithelial cells (PEECs) and evaluate Mo toxicity and its potential molecular mechanisms, Mo-treated PEECs models were established by incubating the cells with various concentrations of medium containing Mo (0, 0.005, 0.020, 0.200, and 5 mmol/L MoNa2O4·2H2O). The results showed that Mo disrupted the morphology and ultrastructure of PEECs, triggered blurred cell edges, cell swelling, cell cycle arrest, and increased apoptosis. At the molecular level, Mo treatment activated the TGF-β1/SMAD2 and PI3K/AKT1 pathways, causing a significant increase in matrix metalloproteinase (MMP)-9 and MMP-2 protein expression. Accompanied by markedly increased tissue inhibitors matrix metalloproteinase (TIMP)-2 and decreased TIMP-1, the balance of MMP2/TIMP-2 and MMP-9/TIMP-1 were disrupted. Ultimately, the receptivity of PEECs was destroyed by excessive Mo, which is revealed by the significant decrease of receptive marker molecules, including leukemia inhibitory factor (LIF), integrins β3 (ITGβ3), heparin-binding epidermal growth factor (HB-EGF), and vascular endothelial growth factor (VEGF). To sum up, the current study demonstrated the potential toxicity of Mo to PEECs, indicating reproductive toxicity at high Mo concentrations and suggesting that the content of Mo should be evaluated as a potential risk factor.
Insights
High molybdenum (Mo) concentrations harm porcine endometrial epithelial cells (PEECs), disrupting cell structure and function. This trace element toxicity impacts reproductive health by reducing key receptive molecules.
Area of Science:
- Reproductive Biology
- Toxicology
- Cell Biology
Background:
- Molybdenum (Mo) is an essential trace element, but its effects on reproductive tissues are not fully understood.
- Porcine endometrial epithelial cells (PEECs) are crucial for embryo implantation and reproductive success.
Purpose of the Study:
- To investigate the impact of varying molybdenum concentrations on PEEC receptivity.
- To evaluate molybdenum toxicity and elucidate its molecular mechanisms in PEECs.
Main Methods:
- Established PEEC models exposed to different concentrations of molybdenum.
- Analyzed cellular morphology, cell cycle, apoptosis, and protein expression of key signaling pathways and matrix metalloproteinases (MMPs).
Main Results:
- Molybdenum disrupted PEEC morphology, induced cell cycle arrest, and increased apoptosis.
- Activated TGF-β1/SMAD2 and PI3K/AKT1 pathways, altering MMPs and their inhibitors (TIMPs), thus disrupting the MMP/TIMP balance.
- Significantly decreased expression of receptive markers: leukemia inhibitory factor (LIF), integrins β3 (ITGβ3), heparin-binding epidermal growth factor (HB-EGF), and vascular endothelial growth factor (VEGF).
Conclusions:
- Excessive molybdenum exhibits toxicity to PEECs, impairing endometrial receptivity.
- High molybdenum concentrations pose a risk to reproductive health, necessitating evaluation as a potential risk factor.
