Journal
JOURNAL OF ENDODONTICS
Volume 41, Issue 7, Pages 1048-1055Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.joen.2015.01.009
Keywords
Ca(v)1.2; DCT; L-type calcium channel; rat dental pulp stem cells
Categories
Funding
- National Natural Science Foundation of China [81070825, 81170951]
- Shanghai Committee of Science and Technology, China [10411964600]
Ask authors/readers for more resources
Introduction: L-type calcium channel (LTCC) is a unique and important factor in several cell lineages, whereas its role in the differentiation of dental pulp stem cells (DPSCs) is not well-known. In this study, we examined the function of LTCC alpha 1C subunit (Ca(v)1.2) and its distal C-terminus (DCT) during the in vitro differentiation of rat DPSCs (rDPSCs). Methods: After fluorescence-activated cell sorting, rDPSCs were differentiated toward dentin sialophosphoprotein positive odontoblasts and neural cells, expressing specific neuronal markers. The inhibition of rDPSC differentiation via LTCC blocker nimodipine and Ca(v)1.2 knockdown through short hairpin RNA was evaluated by using quantitative real-time polymerase chain reaction, Western blot, and immunofluorescence staining. Results: Nimodipine treatment and Ca(v)1.2 knockdown generated similar results. The number of positive calcium nodules and the protein and mRNA levels of dentin sialophosphoprotein were significantly reduced during odontogenic differentiation. The levels of microtubule-associated protein-2 and beta-III-tubulin were reduced in neural differentiation. The expression of DCT decreased after odontogenic differentiation but significantly increased after neural differentiation (P < .05, n = 9). Conclusions: Our data showed that LTCC blocker nimodipine inhibits the odontogenic and neural differentiation of rDPSCs, and Ca(v)1.2 is responsible for the activity of LTCC. The expression of DCT of Ca(v)1.2 significantly changes during both odontogenic and neural differentiation. Thus, Ca(v)1.2 of LTCC plays an essential role in differentiation of DPSCs, which might be mediated through the regulation of DCT levels in DPSCs.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available