mTORC1 promotes mineralization via p53 pathway

The objectives of our study were to investigate the roles mTORC1 in odontoblast proliferation and mineralization determine mechanism by which regulates mineralization. In vitro, MDPC23 cells treated with rapamycin (10 nmol/L) transfected a lentivirus for short hairpin (shRNA)-mediated silencing tuberous sclerosis complex (shTSC1) inhibit activate mTORC1, respectively. CCK8 assays, flow cytometry, Alizarin red S staining, ALP qRT-PCR, western blot analysis performed. TSC1-conditional knockout (DMP1-Cre+; TSC1f/f, hereafter CKO) mice littermate control (DMP1-Cre−; WT) generated. H&E immunofluorescence, micro-CT Transcriptome sequencing was used screen this process. inactivation decreased cell proliferation. qRT-PCR results showed that mineralization-related genes proteins downregulated mTORC1-inactivated cells. Moreover, overactivation promoted gene protein expression. vivo, DV/TV dentin thickness higher CKO than controls staining same results. Mineralization-related expression upregulated. revealed p53 pathway-associated differentially expressed TSC1-deficient By inhibiting alone or both inhibitor, we elucidated acts downstream thereby promotes Taken together, findings demonstrate role mineralization, confirm upregulates via pathway.