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Sphingosine‐1‐phosphate mediates AKT / ERK maintenance of dental pulp homoeostasis
Author(s) -
Pan H. Y.,
Yang H.,
Shao M. Y.,
Xu J.,
Zhang P.,
Cheng R.,
Hu T.
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.12335
Subject(s) - protein kinase b , mapk/erk pathway , western blot , apoptosis , biology , microbiology and biotechnology , kinase , cell growth , signal transduction , biochemistry , gene
Aim To investigate the cell status of dental pulp cells ( DPC s) in a sphingosine‐1‐phosphate ( S 1 P )‐induced microinflammation environment and the possible mechanisms of cell homoeostasis maintenance by S 1 P . Methodology Sphingosine‐1‐phosphate receptor (S1 PR ) expression was examined in DPC s within a local S1P‐induced microinflammation model established using 1 μmol L −1 S 1 P . U 0126 [extracellular signal‐regulated kinase ( ERK ) inhibitor], LY 294002 ( AKT inhibitor) and Y 27632 ( ROCK inhibitor) were used to inhibit corresponding signalling pathways of DPC s. CCK 8 and cell cycle analysis tested cell proliferation. Immunofluorescence staining JC ‐1 detected changes of mitochondrial membrane potential (ΔΨm). Tests for apoptosis and the apoptosis‐related proteins B ax and B cl‐2 were assessed by flow cytometry and western blot analysis, respectively. Expressions of ERK and AKT were evaluated by western blot analysis. The results were analysed using the Student's t‐test and the significance level set at P < 0.05. Results Expressions of S 1 PR 1, S 1 PR 2 and S 1 PR 3 in DPC s differed amongst individuals. DPC s maintained self‐homoeostasis in response to S 1 P ‐induced microinflammation via S 1 PR s. During this repair process, ERK , AKT and ROCK had a short‐term complementary interaction at 60 min, but then AKT and ERK gradually played decisive roles after 24 h in proliferation enhancement and apoptosis inhibition, respectively ( P > 0.05). Conclusions The AKT – ERK balance may determine whether DPC homoeostasis in S 1 P ‐induced microinflammation is maintained by synergistic regulation of cell growth and apoptosis.