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Role of the p38 pathway in mineral trioxide aggregate‐induced cell viability and angiogenesis‐related proteins of dental pulp cell in vitro
Author(s) -
Huang S.C.,
Wu B.C.,
Kao C.T.,
Huang T.H.,
Hung C.J.,
Shie M.Y.
Publication year - 2015
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.12305
Subject(s) - mineral trioxide aggregate , viability assay , p38 mitogen activated protein kinases , angiogenesis , pulp (tooth) , pulp capping , chemistry , in vitro , microbiology and biotechnology , mapk/erk pathway , materials science , kinase , biochemistry , biology , dentistry , medicine , cancer research
Aim To investigate the influence of mineral trioxide aggregate (MTA) on angiogenesis of primary human dental pulp cells ( hDPC s) via the MAPK pathway, in particular p38. Methodology Human dental pulp cells were cultured with MTA to angiogenesis, after which cell viability, ion concentration, osmolality, NO secretion, the von Willebrand factor (v WF ) and angiopoietin‐1 (Ang‐1) protein expression were examined. PrestoBlue ® was used for evaluating the proliferation of hDPC s. An enzyme‐linked immunosorbent assay was employed to determine v WF and Ang‐1 protein secretion in h DPC s cultured on MTA and the control. Cells cultured on the tissue culture plate without the cement were used as the control. The t ‐test was used to evaluate the significance of the differences between the mean values. Results Mineral trioxide aggregate elicited a significant ( P < 0.05) increased viability compared with the control (15%, 16% and 13% on days 1, 3 and 5 of cell seeding, respectively). MTA consumed calcium and phosphate ions, and released more Si ions in the medium. MTA significantly ( P < 0.05) increased the osmolality of the medium to 313, 328 and 341 mOsm kg −1 after 1, 3 and 5 days, respectively. P38 was activated through phosphorylation, and the phosphorylation kinase was investigated in the cell system after being cultured with MTA. Expression levels for Ang‐1 and v WF in hDPC s on MTA were higher than those of the MTA + p38 inhibitor (SB203580) group ( P < 0.05) at all of the time‐points. Conclusions Mineral trioxide aggregate was able to activate the p38 pathway in h DPC s cultured in vitro . Moreover, Si increased the osmolality required to facilitate the angiogenic differentiation of h DPC s via the p38 signalling pathway. When the p38 pathway was blocked by SB203580, the angiogenic‐dependent protein secretion decreased. These findings verify that the p38 pathway plays a key role in regulating the angiogenic behaviour of h DPC s cultured on MTA.