The Anti-Inflammatory Effect of Human Telomerase-Derived Peptide onP. gingivalisLipopolysaccharide-Induced Inflammatory Cytokine Production and Its Mechanism in Human Dental Pulp Cells

Author:

Ko Yoo-Jin1,Kwon Kil-Young2,Kum Kee-Yeon1,Lee Woo-Cheol1,Baek Seung-Ho1,Kang Mo K.3,Shon Won-Jun1

Affiliation:

1. Department of Conservative Dentistry, Dental Research Institute and School of Dentistry, Seoul National University, Jongno-gu, Yeongun-dong 275-1, Seoul 110-749, Republic of Korea

2. Department of Family Medicine, Eulji University School of Medicine, Joong-gu, Yongdu-dong 143-5, Daejeon, Republic of Korea

3. School of Dentistry, David Geffen School of Medicine, Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, CA 90095, USA

Abstract

Porphyromonas gingivalisis considered with inducing pulpal inflammation and has lipopolysaccharide (LPS) as an inflammatory stimulator. GV1001 peptide has anticancer and anti-inflammation activity due to inhibiting activation of signaling molecules after penetration into the various types of cells. Therefore, this study examined inhibitory effect of GV1001 on dental pulp cells (hDPCs) stimulated byP. gingivalisLPS. The intracellular distribution of GV1001 was analyzed by confocal microscopy. Real-time RT-PCR was performed to determine the expression levels of TNF-αand IL-6 cytokines. The role of signaling by MAP kinases (ERK and p38) was explored using Western blot analysis. The effect of GV1001 peptide on hDPCs viability was measured by MTT assay. GV1001 was predominantly located in hDPC cytoplasm. The peptide inhibitedP. gingivalisLPS-induced TNF-αand IL-6 production in hDPCs without significant cytotoxicity. Furthermore, GV1001 treatment markedly inhibited the phosphorylation of MAP kinases (ERK and p38) in LPS-stimulated hDPCs. GV1001 may preventP. gingivalisLPS-induced inflammation of apical tissue. Also, these findings provide mechanistic insight into how GV1001 peptide causes anti-inflammatory actions in LPS-stimulated pulpitis without significantly affecting cell viability.

Funder

Seoul National University Dental Hospital

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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