MiR-322 treatment rescues cell apoptosis and neural tube defect formation through silencing NADPH oxidase 4.

ABSTRACT:

Aims

Failure of neural tube closure resulting from excessive apoptosis leads to neural tube defects (NTDs). NADPH oxidase 4 (NOX4) is a critical mediator of cell growth and death, yet its role in NTDs has never been characterized. NOX4 is a potential target of miR-322, and we have previously demonstrated that miR-322 was involved in high glucose-induced NTDs. In this study, we investigated the effect of NOX4 on the embryonic neuroepithelium in NTDs and reveal a new regulatory mechanism for miR-322 that disrupts neurulation by ameliorating cell apoptosis.

Methods

All-trans-retinoic acid (ATRA)-induced mouse model was utilized to study NTDs. RNA pull-down and dual-luciferase reporter assays were used to confirm the interaction between NOX4 and miR-322. In mouse neural stem cel

SUBMITTER: Liu YS 

PROVIDER: S-EPMC7415201 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature