Sphingosine‐1‐phosphate mediates AKT/ERK maintenance of dental pulp homoeostasis. (15th July 2014)

• Record Type: Journal Article
• Authors: Pan, H. Y.; Yang, H.; Shao, M. Y.; Xu, J.; Zhang, P.; Cheng, R.; Hu, T.
• Is Part Of: International endontic journal. Volume 48:Number 5(2015:May)
• Page Start: 460
• Page End: 468
• Publication Date: 2014-07-15
• Subjects: Endodontics -- Periodicals; 617.6342
• DOI: 10.1111/iej.12335
• Languages: English
• ISSNs: 0143-2885

Abstract

<abstract abstract-type="main" id="iej12335-abs-0001"> <title>Abstract</title> <sec id="iej12335-sec-0001" sec-type="section"> <title>Aim</title> <p>To investigate the cell status of dental pulp cells (DPCs) in a sphingosine‐1‐phosphate (S1P)‐induced microinflammation environment and the possible mechanisms of cell homoeostasis maintenance by S1P.</p> </sec> <sec id="iej12335-sec-0002" sec-type="section"> <title>Methodology</title> <p>Sphingosine‐1‐phosphate receptor (S1PR) expression was examined in DPCs within a local S1P‐induced microinflammation model established using 1 μmol L<sup>−1</sup> S1P. U0126 [extracellular signal‐regulated kinase (ERK) inhibitor], LY294002 (AKT inhibitor) and Y27632 (ROCK inhibitor) were used to inhibit corresponding signalling pathways of DPCs. CCK8 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 Bax and Bcl‐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 <italic>t‐test</italic> and the significance level set at <italic>P </italic><<italic> </italic>0.05.</p> </sec> <sec id="iej12335-sec-0003" sec-type="section"> <title>Results</title> <p>Expressions of S1PR1, S1PR2 and S1PR3 in DPCs differed amongst individuals. DPCs maintained self‐homoeostasis in response to S1P‐induced microinflammation via S1PRs. 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 (<italic>P</italic> > 0.05).</p> </sec> <sec id="iej12335-sec-0004" sec-type="section"> <title>Conclusions</title> <p>The AKT–ERK balance may determine whether DPC homoeostasis in S1P‐induced microinflammation is maintained by synergistic regulation of cell growth and apoptosis.</p> </sec> </abstract>