Abstract：
BACKGROUND AND OBJECTIVE:Dental pulp repair is a common process triggered by microbial and mechanical challenges. Matricellular modulators, such as periostin, are key for extracellular matrix stability and tissue healing. In the scope of the dental pulp, periostin expression has been reported during development and active dentinogenesis. However, the specific dental pulp cell population capable of expressing periostin in response to known regulators has not been clearly defined. Among the different relevant cell populations (i.e., stem cells, fibroblasts and pre-odontoblasts) potentially responsible for periostin expression in the dental pulp, this study aimed to determine which is the primary responder to periostin regulators. METHODS:Human dental pulp stem cells (DPSCs), human dental pulp fibroblasts (DPFs), and rat odontoblast-like cells (MDPC-23) were treated with different concentrations of TGF-β1 or different regimens of biomechanical stimulation to evaluate periostin expression by qRT-PCR, Western blot and ELISA. Statistical analyses were performed by Student's t-test and ANOVA with Fisher's LSD post hoc tests (p ≤ 0.05). RESULTS:DPSC and MDPC-23 showed a statistically significant increase in periostin mRNA expression after exposure to TGF-β1 for 48 h. TGF-β1 also up-regulated periostin protein levels in DPSC. However, periostin significantly down-regulated protein expression in DPF. Different regimens of biomechanical stimulation showed different patterns in protein and mRNA periostin expression. CONCLUSIONS:Expression of periostin was identified in each of the analysed dental pulp cell lines, which can be regulated by TGF-β1 and biomechanical stimulation. Overall, DPSCs are the most responsive cells to stimulation.
journal_name
Arch Oral Bioljournal_title
Archives of oral biologyauthors
Wiesen RM,Padial-Molina M,Volk SL,McDonald N,Chiego D Jr,Botero T,Rios HFdoi
10.1016/j.archoralbio.2015.02.008subject
Has Abstractpub_date
2015-05-01 00:00:00pages
760-7issue
5eissn
0003-9969issn
1879-1506pii
S0003-9969(15)00034-5journal_volume
60pub_type
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