| Title | Plasminogen Activator Inhibitor Type 1 Expression Induced by Lipopolysaccharide of Porphyromonas gingivalis in Human Gingival Fibroblast |
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| Author | Hee Sam Na1, Eun J. Lim1, So Y. Jeong1, Mi H. Ryu2, Mi Hee Park1, and Jin Chung1* |
| Address | 1Department of Oral Microbiology, School of Dentistry, Pusan National University, Yangsan 626-810, Republic of Korea, 2Department of Oral Pathology, School of Dentistry, Pusan National University, Yangsan 626-810, Republic of Korea |
| Bibliography | Journal of Microbiology, 52(2),154-160, 2014, |
| DOI | 10.1007/s12275-014-3022-7 |
| Key Words | Porphyromonas gingivalis, PAI-1, periodontitis |
| Abstract | In the gingival tissues of patients with periodontitis, inflammatory responses are mediated by a wide variety of genes. In our previous screening study, plasminogen activator inhibitor type 1 (PAI-1) mRNA binding protein expression was increased in gingiva from periodontitis patients. In this study, we further investigated the signaling pathway involved in PAI-1 expression induced by Porphyromonas gingivalis LPS (Pg LPS) in human gingival fibroblasts (HGF). When HGFs were treated with Pg LPS, both PAI-1 mRNA expression and PAI-1 protein were induced in a dose-dependent manner. Pg LPS induced NF-κB activation and the expressions of PAI-1 mRNA and protein were suppressed by pretreating with a NF-κB inhibitor. Pg LPS also induced ERK, p38, and JNK activation, and Pg LPS-induced PAI-1 expression was inhibited by ERK/p38/JNK inhibitor pretreatment. In conclusion, Pg LPS induced PAI-1 expression through NF-κB and MAP kinases activation in HGF. |