Ero1 Regulates Alc Calcium Homeostasis In Endoplasmic Reticulum Stress Response

This study aims to explore the role and mechanism of Ero1α in regulating the expression of enamel-related proteins, enamal matrix serine protease and calcium ion distribution during endoplasmic reticulum stress in ALC cells. High-expression endoplasmic reticulum-related proteins were screened through fluoride-treated ameloblast proteomics analysis. An enamel mineralization disorder animal model was established by feeding mice with different concentrations of fluoride in drinking water. Immunofluorescence was used to observe Ero1α expression. qRT-PCR and Western Blot were employed to detect Ero1α expression changes in ameloblasts treated with tunicamycin, sodium fluoride, and 4-phenylbut yrate. Ero1α overexpression and knockdown cell lines were constructed, and qRT-PCR was used to assess changes in enamel-related proteins and proteases. Calcium ion signaling was measured to determine changes in endoplasmic reticulum and mitochondrial calcium flux in Ero1α-overexpressing or knockdown ameloblasts. Proteomics analysis identified highly expressed Ero1α as the target molecule, WB and qRT-PCR showed that Ero1α and GRP78 expression significantly increased in ALC cells treated with fluoride and tunicamycin, which was alleviated by 4-PBA (p < 0.05). Ero1α overexpression and knockdown cell lines were successfully constructed, and WB/qPCR revealed significant effects of Ero1α expression changes on enamel-related proteins (p < 0.05). Calcium ion signaling showed significant changes in calcium flux with altered Ero1α expression (p < 0.05). Ero1α expression increases during endoplasmic reticulum stress in ALC cells, influencing enamel-related proteins, proteases, and calcium ion flux.