Glycoprotein Nonmetastatic Melanoma Protein B (GPNMB) Ameliorates the Inflammatory Response in Periodontal Disease
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ORIGINAL ARTICLE
Glycoprotein Nonmetastatic Melanoma Protein B (GPNMB) Ameliorates the Inflammatory Response in Periodontal Disease Rong Song1,2 and Lexun Lin
2,3
Glycoprotein nonmetastatic melanoma protein B (GPNMB) is a type I transmembrane protein that can modulate osteoblasts and bone mineralization. Periodontal disease (PD) is characterized by gum inflammation, alveolar bone resorption, and tooth loss. In this study, we found that GPNMB is highly expressed in inflamed periodontal tissue through microarray and immunohistochemistry (IHC) assays. The role of GPNMB in the pathogenesis of PD was evaluated with primary human periodontal ligament cells (hPDLCs) treated with lipopolysaccharide (LPS) and a GPNMB-expressing lentivirus (lenti-GP). In the hPDLCs treated with LPS and lenti-GP, the expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 was suppressed and that of IL-10 was upregulated. GPNMB significantly decreased apoptosis in the hPDLCs treated with LPS. GPNMB could upregulate the expression of Jumonji domain-containing protein 3 (Jmjd3), a histone 3 lysine 27 (H3K27) demethylase that is linked to the modulation of the inflammatory response and apoptosis. Taken together, our data find that GPNMB is highly expressed in gum tissue with PD and may be an anti-inflammatory player in the pathogenesis of PD.
Abstract—
KEY WORDS: periodontal disease; GPNMB; inflammatory cytokine; Jmjd3.
INTRODUCTION Periodontal disease (PD) is a chronic oral disease that is highly prevalent in adults. PD is mainly characterized by inflammation in the gums, periodontal pocket formation, alveolar bone resorption, and tooth loosening and displacement [1, 2]. There are two hallmark events in PD: inflammation and alveolar bone resorption/tooth loss [2, 3]. The inflammation event includes gingivitis and periodontitis 1
Department of Prosthodontics, First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China 2 Department of Microbiology, Harbin Medical University, Harbin, 150081, China 3 To whom correspondence should be addressed at Department of Microbiology, Harbin Medical University, Harbin, 150081, China. E-mail: [email protected]
[3]. In this study, our initial intention was to probe the molecular basis for bone destruction during PD. A microarray screening bone metabolism factors was used to assess gum tissue samples collected from patients who suffered from PD. In the microarray, glycoprotein nonmetastatic melanoma protein B (GPNMB), monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), and macrophage colony-stimulating factor (MCSF) showed varied expression patterns between the healthy and inflamed periodontal tissues. MCP-1, MIP-1α, and MCSF are well established as inflammatory cytokines [4–7]. To date, there are no data available on the connection between GPNMB and the pathogenesis of PD. GPNMB, a type I transmembrane protein with 560– 572 amino acids, is also known as osteoactivin (OA) in rats and dendritic cell-heparin integrin ligand (DC-HIL) in mice [8–10].
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