Retinoid acid-induced microRNA-31-5p suppresses myogenic proliferation and differentiation by targeting CamkII?.

ABSTRACT: We previously reported that Wnt5a/CaMKII? (calcium/calmodulin-dependent protein kinase II delta) pathway was involved in the embryonic tongue deformity induced by excess retinoic acid (RA). Our latest study found that the expression of miR-31-5p, which was predicted to target the 3'UTR of CamkII?, was raised in the RA-treated embryonic tongue. Thus, we hypothesized that the excess RA regulated Wnt5a/CaMKII? pathway through miR-31-5p in embryonic tongue.C2C12 myoblast line was employed as an in vitro model to examine the suppression of miR-31-5p on CamkII? expression, through which RA impaired the myoblast proliferation and differentiation in embryonic tongue.RA stimulated the expression of miR-31-5p in both embryonic tongue and C2C12 myoblasts. Luciferase reporter assay confirmed that the 3'UTR of CamkII? was a target of miR-31-5p. MiR-31-5p mimics disrupted CamkII? expression, C2C12 proliferation and differentiation as excess RA did, while miR-31-5p inhibitor partially rescued these defects in the presence of RA.Excess RA can stimulate miR-31-5p expression to suppress CamkII?, which represses the proliferation and differentiation of tongue myoblasts.

SUBMITTER: Liu B 

PROVIDER: S-EPMC5437717 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature