Effect of lipopolysaccharide on proliferation and inflammatory factors expression of human periodontal ligament stem cells.
- Author:
Lan WANG
1
;
Jiajia XIA
;
Qi LIU
;
Yan JIN
Author Information
- Publication Type:Journal Article
- MeSH: Cell Differentiation; Humans; Interleukin-1beta; Interleukin-6; Lipopolysaccharides; Monocytes; Organic Chemicals; Periodontal Ligament; Porphyromonas gingivalis; RNA, Messenger; Stem Cells; Tumor Necrosis Factor-alpha
- From: West China Journal of Stomatology 2013;31(3):286-290
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of Porphyromonas gingivalis lipopolysaccharide (LPS) on proliferation and inflammatory factors expression of human periodontal ligament stem cells (HPDLSCs).
METHODSHPDLSCs were cultivated and identified. Experiment was divided into 3 groups according to culture solution: Group A with alpha-MEM culture solution containing 10 microg.mL-1 LPS, group B with supernatant fluid containing 10ng.mL-1 LPS stimulated monocyte, group C with alpha-MEM culture solution. The proliferation ability of HPDLSCs was analyzed by MTF assay. The expression levels of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha) mRNA of HPDLSCs were detected by reverse transcriptase polymerase chain reaction(RT-PCR).
RESULTSHPDLSCs had clonality, bone and fat differentiation ability. Compared with group C, the proliferation ability of HPDLSCs of group A and group B was significantly inhibited, and the proliferation ability of HPDLSCs of group B were more significantly inhibited than that of group A (P<0.05). The expression of IL-1beta, IL-6 and TNF-alpha mRNA of group A and group B increased compared with the control group, and the expression of IL-1beta, IL-6 and TNF-alpha mRNA of group B increased more than that of group A (P<0.05).
CONCLUSIONPorphyromonas gingivalis may inhibit the proliferation of HPDLSCs directly or indirectly through LPS and increase expression of inflammatory factor, exacerbate periodontal inflammatory tissue damage and delay the self-repairing of periodontal tissue.