ClC-5 regulates dentin development through TGF-β1 pathway
Copyright policy )ClC-5 regulates dentin development through TGF-β1 pathway
ClC-5 is one of the voltage-dependent chloride channel (ClC) family members. Mutations involving CLCN5 cause an X-linked nephropathy associated with Dent's disease. Some Clcn5 gene knockout (ClC-5 KO) mice have abnormal growth of the teeth; however, the expression and function of ClC-5 during tooth development is still unknown. Herein we report abnormal dentin structure, decreased DSPP and increased TGF-beta1 protein level in ClC-5 KO teeth. In odontoblast-like MDPC-23 cells, the mRNA levels of Tgfb1, Dspp and Dmp-1 were upregulated with Clcn5 RNAi after 48h treatment; whilst there was no change in those of TGF-beta receptor Tgfbr1 and Tgfbr2. We suggest that the dentin changes in ClC-5 KO mice might be a result of increasing TGF-beta1, and the interplay between ClC-5 and TGF-beta1 needs further identified.
- Air Force Medical University China (People's Republic of)
Mice, Knockout, Extracellular Matrix Proteins, Odontoblasts, Sialoglycoproteins, Gene Expression, Tooth Germ, Phosphoproteins, Up-Regulation, Transforming Growth Factor beta1, Mice, Animals, Newborn, Chloride Channels, Dentin, Animals, RNA Interference, Cells, Cultured
Mice, Knockout, Extracellular Matrix Proteins, Odontoblasts, Sialoglycoproteins, Gene Expression, Tooth Germ, Phosphoproteins, Up-Regulation, Transforming Growth Factor beta1, Mice, Animals, Newborn, Chloride Channels, Dentin, Animals, RNA Interference, Cells, Cultured
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