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Porphyromonas gingivalis Lipopolysaccharide Stimulation of Vascular Smooth Muscle Cells Activates Proliferation and Calcification
Author(s) -
Liu Guirong,
Deng Jing,
Zhang Qiang,
Song Wenbin,
Chen Shulan,
Lou Xiuxiu,
Zhang Pengmei,
Pan Keqing
Publication year - 2016
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2016.150602
Subject(s) - vascular smooth muscle , porphyromonas gingivalis , bone sialoprotein , osteopontin , alkaline phosphatase , calcification , endocrinology , matrix gla protein , chemistry , medicine , lipopolysaccharide , biology , microbiology and biotechnology , ectopic calcification , biochemistry , periodontitis , osteocalcin , smooth muscle , enzyme
Background: Porphyromonas gingivalis ( Pg ) is a major etiologic agent of periodontitis, whose virulence has been attributed to different factors, including lipopolysaccharide (LPS). Vascular ectopic calcification as a well‐known major risk factor for adverse cardiovascular diseases is a highly prevalent vascular pathophenotype, and vascular smooth muscle cells (VSMCs) play an important role in mediating vascular calcification. It was hypothesized that Pg ‐LPS may stimulate vascular calcification through a direct effect on VSMC function. To test this hypothesis, the effect of Pg ‐LPS on VSMC calcification was determined. Methods: Primary cultures of VSMCs were obtained and identified by immunochemistry in vitro. The proliferation and alkaline phosphatase (ALP) activity of VSMCs were measured using a cell counting kit and an ALP activity test. Mineral deposition was examined using alizarin red staining. Gene (e.g. ALP , core binding factor α1 [ Cbfα1 ], bone sialoprotein [ BSP ], and osteopontin [ OPN ]) expression levels altered by Pg ‐LPS were determined by reverse transcription‐polymerase chain reaction array. Results: Pg ‐LPS could increase the proliferation of VSMCs at different times and enhance ALP activity of VSMCs after 1 day. Alizarin red staining and quantification showed that, with Pg ‐LPS treatment, VSMCs displayed more obvious calcification nodules. When stimulated with Pg ‐LPS, the expression of specific osteogenic genes (e.g., ALP , Cbfα1 , BSP , and OPN ) was significantly promoted in the presence or absence of mineralization‐inducing medium, whereas the expression of the OPN gene was inhibited in the mineralization induction group at day 7. Conclusion: Pg ‐LPS can stimulate VSMC calcification, which results in vascular calcification, further proving the precise relationship between periodontitis and vascular calcification.