Store-operated Ca²⁺ entry controls ameloblast cell function and enamel development.

ABSTRACT: Loss-of-function mutations in stromal interaction molecule 1 (STIM1) impair the activation of Ca²⁺ release-activated Ca²⁺ (CRAC) channels and store-operated Ca²⁺ entry (SOCE), resulting in a disease syndrome called CRAC channelopathy that is characterized by severe dental enamel defects. The cause of these enamel defects has remained unclear given a lack of animal models. We generated Stim1/2^K14cre mice to delete STIM1 and its homolog STIM2 in enamel cells. These mice showed impaired SOCE in enamel cells. Enamel in Stim1/2^K14cre mice was hypomineralized with decreased Ca content, mechanically weak, and thinner. The morphology of SOCE-deficient ameloblasts was altered, showing loss of the typical ruffled border, resulting

SUBMITTER: Eckstein M 

PROVIDER: S-EPMC5358480 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature