当前位置： SCI文献检索 > ARCHIVES OF ORAL BIOLOGY期刊下所有文献 > IL-6 regulates stress-induced REX-1 expression via ATP-P2Y1 signalling in stem cells isolated from human exfoliated deciduous teeth.

IL-6 regulates stress-induced REX-1 expression via ATP-P2Y1 signalling in stem cells isolated from human exfoliated deciduous teeth.

Abstract：

OBJECTIVE:To investigate the relationship between ATP and IL-6 in mechanical stress-induced REX-1 expression in SHEDs. METHODS:Cells were stimulated with mechanical stress (0-2.5 gcm(-2)), IL-6 (0.1-5 ng/ml), or ATP (10-100 μM) for 2h in serum-free media. IL-6 and REX-1 expression was examined by qualitative and quantitative polymerase chain reaction. ATP release was measured using a bioluminescence assay. The molecular mechanisms of the signalling pathways were investigated using chemical inhibitors. RESULTS:Mechanical stress induced IL-6 and REX-1 mRNA expression and ATP release. JAK inhibitor I inhibited the increase in REX-1 expression and ATP release but not IL-6 induction. Furthermore, suramin inhibited the upregulation of REX-1 mRNA expression but not ATP release. Exogenous IL-6 promoted both ATP release and REX-1 expression. The IL-6-induced REX-1 expression was attenuated by a P2Y1-specific receptor antagonist. Moreover, REX-1 expression was upregulated in a dose-dependent manner by the addition of ATP or a P2Y1 agonist. This inductive effect was abolished by the P2Y1-specific receptor antagonist. CONCLUSIONS:ATP-P2Y1 signalling is involved in IL-6-regulated stress-induced REX-1 expression in SHEDs. These results imply the participation of mechanical stress, IL-6, and ATP in regulating the expression of REX-1, a pluripotent stem cell marker.

journal_name

Arch Oral Biol

journal_title

Archives of oral biology

authors

Govitvattana N,Osathanon T,Toemthong T,Pavasant P

doi

10.1016/j.archoralbio.2014.09.008

subject

Has Abstract

pub_date

2015-01-01 00:00:00

pages

160-6

issue

1

eissn

0003-9969

issn

1879-1506

pii

S0003-9969(14)00249-0

journal_volume

60

pub_type

杂志文章

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