Format

Send to

Choose Destination
J Endod. 2018 May;44(5):786-791. doi: 10.1016/j.joen.2017.12.023. Epub 2018 Mar 15.

FoxO3a Regulates Inflammation-induced Autophagy in Odontoblasts.

Author information

1
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory for Oral Biomedicine of Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, Wuhan, China.
2
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory for Oral Biomedicine of Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, Wuhan, China; Department of Endodontics, School and Hospital of Stomatology, Wuhan University, Wuhan, China. Electronic address: luzhang2012@whu.edu.cn.

Abstract

INTRODUCTION:

FoxO3a is a member of FoxO transcription factor family that participates in the transcriptional regulation of autophagy. In this study we explored the anti-inflammatory function of FoxO3a-regulated autophagy in inflamed human dental pulp and lipopolysaccharide-treated mDPC6T cells.

METHODS:

The expression of FoxO3a and autophagy markers in caries and pulpitis from human dental pulp were examined by immunohistochemistry and Western blot. We conducted in vitro studies by treating mDPC6T cells with lipopolysaccharide for various lengths of time. Next, we measured the nuclear translocation of FoxO3a by immunofluorescence and investigated the potential relationship between FoxO3a and autophagy after FoxO3a knockdown using small interfering RNA.

RESULTS:

The expression of FoxO3a and autophagy proteins was upregulated in the odontoblasts of human caries and pulpitis samples. In addition, we also observed that the enhanced nuclear translocation of FoxO3a was positively correlated with the progression of inflammation. The results of our in vitro study revealed that 6 hours of lipopolysaccharide treatment increased nuclear translocation of FoxO3a and activated autophagy in mDPC6T cells. We also observed that the knockdown of FoxO3a suppressed autophagy.

CONCLUSIONS:

Our data indicate that FoxO3a might play a role in autophagy activation and the maintenance of intracellular homeostasis in inflamed odontoblasts.

KEYWORDS:

Autophagy; FoxO3a; inflammation; odontoblast

PMID:
29551204
DOI:
10.1016/j.joen.2017.12.023
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center