Oxidized low-density lipoprotein-induced periodontal inflammation is associated with the up-regulation of cyclooxygenase-2 and microsomal prostaglandin synthase 1 in human gingival epithelial cells

Journal Article · Fri Oct 07 04:00:00 EDT 2011 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2011.09.002· OSTI ID:22207514

Nagahama, Yu ^[1]; Obama, Takashi ^[2]; Usui, Michihiko ^[1]; Kanazawa, Yukari ^[2]; Iwamoto, Sanju ^[3]; Suzuki, Kazushige ^[1]; Miyazaki, Akira ^[3]; Yamaguchi, Tomohiro ^[2]; Yamamoto, Matsuo ^[1]; Itabe, Hiroyuki ^[2]

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1. Department of Periodontology, School of Dentistry, Showa University Dental Hospital, Tokyo (Japan)
2. Department of Biological Chemistry, Showa University School of Pharmacy, Tokyo (Japan)
3. Department of Biochemistry, Showa University School of Medicine, Tokyo (Japan)

Highlights: {yields} OxLDL-induced responses in human gingival epithelial cells were studied. {yields} OxLDL enhanced the production of IL-8, IL-1{beta} and PGE{sub 2} in Ca9-22 cells. {yields} An NF-{kappa}B inhibitor suppressed the expression of COX-2 and mPGES1 induced by oxLDL. {yields} Unlike the case in macrophages, oxLDL did not increase the CD36 level. -- Abstract: Periodontitis is characterized by chronic gingival tissue inflammation, and inflammatory mediators such as IL-8 and prostaglandin E{sub 2} (PGE{sub 2}) are associated with disease progression. Previously we showed that oxidatively modified low-density lipoprotein (oxLDL) was present in gingival crevicular fluid. In this study, the role of oxLDL in the gingival epithelial cell inflammatory response was further investigated using Ca9-22 cells and primary human oral keratinocytes (HOK). Treatment of Ca9-22 cells and HOK with oxLDL induced an up-regulation of IL-8 and the PGE{sub 2}-producing enzymes, cyclooxygenase-2 and microsomal PGE{sub 2} synthase-1. These responses induced by oxLDL were significantly suppressed by a nuclear factor-kappa B (NF-{kappa}B) inhibitor. However, unlike the result in macrophages, oxLDL did not lead to an increase in CD36 expression in these two cells. These results suggest that oxLDL elicits gingival epithelial cell inflammatory responses through an activation of the NF-{kappa}B pathway. These data suggest a mechanistic link between periodontal disease and lipid metabolism-related disorders, including atherosclerosis.

• OSTI ID: 22207514
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 413; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANTIBODIES
ARTERIOSCLEROSIS
CATTLE
CORONARIES
ENZYMES
GENE REGULATION
INFLAMMATION
LECITHINS
LIPOPROTEINS
MACROPHAGES
METABOLISM
OXIDATION
PHOSPHATES
PROSTAGLANDINS