Title |
Porphyromonas gingivalis-Derived Lipopolysaccharide-Mediated Activation of MAPK Signaling Regulates Inflammatory Response and Differentiation in Human Periodontal Ligament Fibroblasts |
Author |
Taegun Seo1, Seho Cha1, Tae-Il Kim2*, Hee-Jung Park2, Jeong-Soon Lee2, and Kyung Mi Woo3 |
Address |
1Department of Life Science, Dongguk University-Seoul, Seoul 100-715, Republic of Korea, 2Department of Periodontology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 110-749, Republic of Korea, 3Department of Cell and Developmental Biology, Seoul National University School of Dentistry, Seoul 110-749, Republic of Korea |
Bibliography |
Journal of Microbiology, 50(2),311-319, 2012,
|
DOI |
|
Key Words |
apoptosis, cell differentiation, lipopolysaccharide, mitogen-activated protein kinase, periodontal ligament, Porphyromonas gingivalis |
Abstract |
Porphyromonas gingivalis (P.g.), which is a potential pathogen
for periodontal diseases, contains lipopolysaccharide
(LPS), and this endotoxin stimulates a variety of cellular
responses. At present, P.g.-derived LPS-induced cellular responses
in human periodontal ligament fibroblasts (PDLFs)
are not well characterized. Here, we demonstrate that P.gderived
LPS regulates inflammatory responses, apoptosis
and differentiation in PDLFs. Interleukin-6 (IL-6) and -8
(IL-8) were effectively upregulated by treatment of P.g.-derived
LPS, and we confirmed apoptosis markers including
elevated cytochrome c levels, active caspase-3 and morphological
change in the presence of P.g.-derived LPS. Moreover,
when PDLFs were cultured with differentiation media, P.g.-
derived LPS reduced the expression of differentiation marker
genes, as well as reducing alkaline phosphatase (ALP) activity
and mineralization. P.g.-derived LPS-mediated these
cellular responses were effectively abolished by treatment
of mitogen-activated protein kinase (MAPK) inhibitors.
Taken together, our results suggest that P.g.-derived LPS
regulates several cellular responses via activation of MAPK
signaling pathways in PDLFs. |