2-Hydroxyethyl methacrylate inhibits migration of dental pulp stem cells.

Abstract:

INTRODUCTION:Cell migration is an important step in pulpal wound healing. Although components in the resin-based dental materials are known to have adverse effects on pulp wound healing including proliferation and mineralization, their effects on cell migration have been scarcely examined. Here, we investigated the effects of 2-hydroxyethyl methacrylate (HEMA) on the migration of dental pulp stem cells (DPSC) in vitro. METHODS:Cell viability was assessed using the MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay, and cell migration was evaluated using the wound scratch assay and transwell migration assay at noncytotoxic doses. The Western blot was used to examine pathways associated with migration such as focal adhesion kinase, mitogen-activated protein kinase, and glycogen synthase kinase 3. RESULTS:There were no drastic changes in the cell viability below 3 mmol/L HEMA. When DPSCs were treated with HEMA at 0.5, 1.0, and 2.5 mmol/L, cell migration was diminished. HEMA-treated DPSCs exhibited the loss of phosphorylated focal adhesion kinase in a dose-dependent manner. The HEMA-mediated inhibition of cell migration was associated with phosphorylation of p38 but not glycogen synthase kinase 3, Extracellular signal-related kinase (ERK), or c-Jun N-terminal kinase (JNK) pathways. When we inhibited the p38 signaling pathway using a p38 inhibitor, the migration of DPSCs was suppressed. CONCLUSIONS:HEMA inhibits the migration of dental pulp cells in vitro, suggesting that poor pulpal wound healing under resin-based dental materials may be caused, in part, by the inhibition of cell migration by HEMA.

journal_name

J Endod

journal_title

Journal of endodontics

authors

Williams DW,Wu H,Oh JE,Fakhar C,Kang MK,Shin KH,Park NH,Kim RH

doi

10.1016/j.joen.2013.06.004

subject

Has Abstract

pub_date

2013-09-01 00:00:00

pages

1156-60

issue

9

eissn

0099-2399

issn

1878-3554

pii

S0099-2399(13)00541-4

journal_volume

39

pub_type

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