Mechanism of neural tube defects caused by ethionine in mice
10.13200/j.cnki.cjb.004043
- VernacularTitle:乙硫氨酸引起小鼠神经管畸形的机制探讨
- Author:
WANG Wenzhuo
- Publication Type:Journal Article
- Keywords:
Neural tube defects(NTDs);
Ethionine;
Migration;
Wnt/β-catenin signaling pathway
- From:
Chinese Journal of Biologicals
2024;37(6):666-671
- CountryChina
- Language:Chinese
-
Abstract:
Objective To prepare a neural tube defects(NTDs)model in mice with the structural analogue of methionineethionine,and investigate the effects of NTDs on the proliferation,apoptosis and migration of nerve cells.Methods Mouse NTDs embryo model was established.The C57BL/6J mice were injected intraperitoneally with 500 mg/kg ethionine after gestation to 7.5 d(E7.5),while the mice in control group were injected with the same dose of normal saline.Mouse embryos were taken at E11.5 and observed under stereomicroscope;The levels of S-adenosylhomocysteine(SAH)and Sadenosylmethionine(SAM)in plasma of pregnant mice were detected by ELISA;Western blot and RT-PCR were used to detect the expression of migration proteins E-cadherin and N-cadherin and the mRNA transcription in embryonic brain tissue.The expression of proliferation protein PCNA and apoptosis protein cleaved-Caspase3,and Wnt/β-catenin signaling pathway marker proteins β-catenin,TCF4 and C-myc were detected by Western blot.Results After the intervention of ethionine,the SAM content in pregnant mice decreased,the SAH content increased,and the SAM/SAH ratio decreased.Compared with the control group,the E-cadherin and cleaved-Caspase 3 were highly expressed and the apoptosis increased in NTDs group;The expression of N-cadherin and PCNA decreased,and the cell proliferation and migration decreased;The low expression of Wnt/β-catenin signaling pathway marker proteins β-catenin,TCF4 and C-myc indicated that the pathway was inhibited.Conclusion Ethionine may cause NTDs by promoting cell apoptosis via inhibiting Wnt/β-catenin signaling pathway and the proliferation and migration of nerve cells.
