C-reactive protein, a disintegrin and metalloproteinase 17 protein, and cathepsin D in chronic periodontitis with type 2 diabetes mellitus
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
The purpose of this study was to compare and quantify the expression of C-reactive protein (CRP), a disintegrin and metalloproteinase 17 (ADAM17) protein, and cathepsin D in the gingival tissues of patients with type 2 diabetes mellitus (DM) with those in healthy adults with chronic periodontitis. Gingival tissue samples were obtained during periodontal surgery or tooth extraction. Depending on the patient’s systemic condition and clinical criteria of gingiva, each gingival sample was divided into three groups. Group 1 (n=12) included clinically healthy gingiva without bleeding and no evidence of bone resorption or periodontal pockets. Group 2 (n=12) included inflamed gingiva from patients with chronic periodontitis. Group 3 (n=12) included inflamed gingiva from patients with chronic periodontitis associated with type 2 DM. Tissue samples were prepared and analyzed using Western blotting. The relative quantifications of CRP, ADAM17 protein, and cathepsin D were performed with a densitometer, and the results were statistically analyzed by one-way analysis of variance followed by Tukey test. The expression levels of CRP, ADAM17 protein, and cathepsin D increased in groups 2 and 3 compared with those in group 1. The differences among three groups were statistically significant ( p <0.05). In conclusion, this study demonstrated that the expression levels of CRP, ADAM17 protein and cathepsin D might act as inflammatory markers in periodontal inflamed tissue. It can be assumed that CRP, ADAM17 protein, and cathepsin D are partly involved in the progression of periodontal inflammation associated with type 2 DM.
Abstract
The purpose of this study was to compare and quantify the expression of C-reactive protein (CRP), a disintegrin and metalloproteinase 17 (ADAM17) protein, and cathepsin D in the gingival tissues of patients with type 2 diabetes mellitus (DM) with those in healthy adults with chronic periodontitis. Gingival tissue samples were obtained during periodontal surgery or tooth extraction. Depending on the patient’s systemic condition and clinical criteria of gingiva, each gingival sample was divided into three groups. Group 1 (n=12) included clinically healthy gingiva without bleeding and no evidence of bone resorption or periodontal pockets. Group 2 (n=12) included inflamed gingiva from patients with chronic periodontitis. Group 3 (n=12) included inflamed gingiva from patients with chronic periodontitis associated with type 2 DM. Tissue samples were prepared and analyzed using Western blotting. The relative quantifications of CRP, ADAM17 protein, and cathepsin D were performed with a densitometer, and the results were statistically analyzed by one-way analysis of variance followed by Tukey test. The expression levels of CRP, ADAM17 protein, and cathepsin D increased in groups 2 and 3 compared with those in group 1. The differences among three groups were statistically significant ( p <0.05). In conclusion, this study demonstrated that the expression levels of CRP, ADAM17 protein and cathepsin D might act as inflammatory markers in periodontal inflamed tissue. It can be assumed that CRP, ADAM17 protein, and cathepsin D are partly involved in the progression of periodontal inflammation associated with type 2 DM.
참고문헌 (53)
- Pourya Gholizadeh, "Oral pathogenesis of Aggregatibacter actinomycetemcomitans", Microbial Pathogenesis, 113, pp.303~311 (2017), Elsevier BV[DOI]
- Sigmund S. Socransky, "Periodontal microbial ecology", Periodontology 2000, 38(1), pp.135~187 (2005), Wiley[DOI]
- Kitti Torrungruang, "Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Treponema denticola", Prevotella intermedia Co-Infection Are Associated with Severe Periodontitis in a Thai Population, 2015, pp.10(8), e0136646~[DOI]
- James D. Beck, "Periodontal profile class is associated with prevalent diabetes, coronary heart disease, stroke, and systemic markers of C-reactive protein and interleukin-6", Journal of Periodontology, 89(2), pp.157~165 (2018), Wiley[DOI]
- Cassio KAMPITS, "Periodontal disease and inflammatory blood cytokines in patients with stable coronary artery disease", Journal of Applied Oral Science, 24(4), pp.352~358 (2016), FapUNIFESP (SciELO)[DOI]
- Barbara Noack, "Periodontal Infections Contribute to Elevated Systemic C-Reactive Protein Level", Journal of Periodontology, 72(9), pp.1221~1227 (2001), Wiley[DOI]
- Salomon Amar, "Periodontal Disease Is Associated With Brachial Artery Endothelial Dysfunction and Systemic Inflammation", Arteriosclerosis, Thrombosis, and Vascular Biology, 23(7), pp.1245~1249 (2003), Ovid Technologies (Wolters Kluwer Health)[DOI]
- K Buhlin, "Risk factors for cardiovascular disease in patients with periodontitis", European Heart Journal, 24(23), pp.2099~2107 (2003), Oxford University Press (OUP)[DOI]
- Ronald G. Craig, "Relationship of Destructive Periodontal Disease to the Acute-Phase Response", Journal of Periodontology, 74(7), pp.1007~1016 (2003), Wiley[DOI]
- Pietilä K, "Serum C-reactive protein and infarct size in myocardial infarct patients with a closed versus an open infarct-related coronary artery after thrombolytic therapy", Eur Heart J, 14, pp.915~919 (1993)[DOI]
- Paul M. Ridker, "Inflammation, Aspirin, and the Risk of Cardiovascular Disease in Apparently Healthy Men", New England Journal of Medicine, 336(14), pp.973~979 (1997), Massachusetts Medical Society[DOI]
- Paul M. Ridker, "On Evolutionary Biology, Inflammation, Infection, and the Causes of Atherosclerosis", Circulation, 105(1), pp.2~4 (2002), Ovid Technologies (Wolters Kluwer Health)[DOI]
- Paul M. Ridker, "Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular Events", New England Journal of Medicine, 347(20), pp.1557~1565 (2002), Massachusetts Medical Society[DOI]
- Paul M Ridker, "C-reactive protein, inflammation, and coronary risk", Cardiology Clinics, 21(3), pp.315~325 (2003), Elsevier BV[DOI]
- Joshua A. Beckman, "Comparison of Usefulness of Inflammatory Markers in Patients With Versus Without Peripheral Arterial Disease in Predicting Adverse Cardiovascular Outcomes (Myocardial Infarction, Stroke, and Death)", The American Journal of Cardiology, 96(10), pp.1374~1378 (2005), Elsevier BV[DOI]
- Augustin Amour, "TNF-α converting enzyme (TACE) is inhibited by TIMP-3", FEBS Letters, 435(1), pp.39~44 (1998), Wiley[DOI]
- Ari Pekka J Huovila, "ADAMs and cell fusion", Current Opinion in Cell Biology, 8(5), pp.692~699 (1996), Elsevier BV[DOI]
- Carl P Blobel, "Metalloprotease-Disintegrins: Links to Cell Adhesion and Cleavage of TNFα and Notch", Cell, 90(4), pp.589~592 (1997), Elsevier BV[DOI]
- M.L. Moss, "Structural features and biochemical properties of TNF-α converting enzyme (TACE)", Journal of Neuroimmunology, 72(2), pp.127~129 (1997), Elsevier BV[DOI]
- Petr Benes, "Cathepsin D—Many functions of one aspartic protease", Critical Reviews in Oncology, 2008, pp.68(1), 12~28[DOI]
- Daniel Baechle, "Cathepsin D Is Present in Human Eccrine Sweat and Involved in the Postsecretory Processing of the Antimicrobial Peptide DCD-1L", Journal of Biological Chemistry, 281(9), pp.5406~5415 (2006), American Society for Biochemistry & Molecular Biology (ASBMB)[DOI]
- Jukka K. Hakala, "Lysosomal Enzymes Are Released From Cultured Human Macrophages, Hydrolyze LDL In Vitro, and Are Present Extracellularly in Human Atherosclerotic Lesions", Arteriosclerosis, Thrombosis, and Vascular Biology, 23(8), pp.1430~1436 (2003), Ovid Technologies (Wolters Kluwer Health)[DOI]
- Wataru Morikawa, "Angiostatin Generation by Cathepsin D Secreted by Human Prostate Carcinoma Cells", Journal of Biological Chemistry, 275(49), pp.38912~38920 (2000), American Society for Biochemistry & Molecular Biology (ASBMB)[DOI]
- Minarowska A, "Regulatory role of cathepsin D in apoptosis", Folia Histochem Cytobiol, 45, pp.159~163 (2007)
- Valérie Laurent-Matha, "Catalytically inactive human cathepsin D triggers fibroblast invasive growth", The Journal of Cell Biology, 168(3), pp.489~499 (2005), Rockefeller University Press[DOI]
- Aruna Vashishta, "Procathepsin D secreted by HaCaT keratinocyte cells – A novel regulator of keratinocyte growth", European Journal of Cell Biology, 86(6), pp.303~313 (2007), Elsevier BV[DOI]
- Olga Schestkowa, "The catalytically inactive precursor of cathepsin D induces apoptosis in human fibroblasts and HeLa cells", Journal of Cellular Biochemistry, 101(6), pp.1558~1566 (2007), Wiley[DOI]
- Ira B. Lamster, "The Relationship Between Oral Health and Diabetes Mellitus", The Journal of the American Dental Association, 139, pp.19S~24S (2008), Elsevier BV[DOI]
- D.T. Graves, "Diabetes-enhanced Inflammation and Apoptosis—Impact on Periodontal Pathology", Journal of Dental Research, 85(1), pp.15~21 (2016), SAGE Publications[DOI]
- Sara G. Grossi, "Periodontal Disease and Diabetes Mellitus: A Two-Way Relationship", Annals of Periodontology, 3(1), pp.51~61 (1998), Wiley[DOI]
- Research, Science and Therapy Committee of The American Academy of Periodontology, "Position Paper: Diabetes and Periodontal Diseases", Journal of Periodontology, 71(4), pp.664~678 (2000), Wiley[DOI]
- Nagata T., "Relationhip between diabetes and periodontal disease", Clin Calcium, 19, pp.1291~1298 (2009)
- Mühlemann HR, "Gingival sulcus bleeding--a leading symptom in initial gingivitis", Helv Odontol Acta, 15, pp.107~113 (1971)
- 박재완, "The comparison of IL-6, elastase and α1-PI expressions in human chronic periodontitis with type 2 diabetes mellitus", Journal of Periodontal & Implant Science, 37(5), pp.325~338 (2007), 대한치주과학회
- 주상돈, "The comparison of inflammatory mediator expression in gingival tissues from human chronic periodontitis patients with and without type 2 diabetes mellitus", Journal of Periodontal & Implant Science, 37(5), pp.353~369 (2007), 대한치주과학회
- J-Y Cho, "Expression and activity of human Na+", I− symporter in human glioma cells by adenovirus-mediated gene delivery, 2000, pp.7(9), 740~749[DOI]
- Garofalo GS, "Relationships between diabetes mellitus and periodontal disease : current knowledges and therapeutic prospects", Clin Ter, 159, pp.97~104 (2008)
- Kasaj A, "The relationship of periodontitis and diabetes mellitus", Acta Med Croatica, 61, pp.369~374 (2007)
- Alves C, "Pathogenic aspects of the periodontal disease associated to diabetes mellitus", Arq Bras Endocrinol Metabol, 51, pp.1050~1057 (2007)
- Lei Chen, "Association of Periodontal Parameters With Metabolic Level and Systemic Inflammatory Markers in Patients With Type 2 Diabetes", Journal of Periodontology, 81(3), pp.364~371 (2010), Wiley[DOI]
- D. E. King, "C-Reactive Protein and Glycemic Control in Adults With Diabetes", Diabetes Care, 26(5), pp.1535~1539 (2003), American Diabetes Association[DOI]
- Aruna D. Pradhan, "C-Reactive Protein, Interleukin 6, and Risk of Developing Type 2 Diabetes Mellitus", JAMA, 286(3), pp.327~ (2001), American Medical Association (AMA)[DOI]
- Gerard J. Linden, "Persistently raised C-reactive protein levels are associated with advanced periodontal disease", Journal of Clinical Periodontology, 35(9), pp.741~747 (2008), Wiley[DOI]
- Stefan Renvert, "Short-Term Effects of an Anti-Inflammatory Treatment on Clinical Parameters and Serum Levels of C-Reactive Protein and Proinflammatory Cytokines in Subjects With Periodontitis", Journal of Periodontology, 80(6), pp.892~900 (2009), Wiley[DOI]
- "Shanghai Kou Qiang Yi Xue", 2009, 132~135
- G.D. Slade, "Acute-phase Inflammatory Response to Periodontal Disease in the US Population", Journal of Dental Research, 79(1), pp.49~57 (2016), SAGE Publications[DOI]
- Willa A. Hsueh, "Peroxisome Proliferator-Activated Receptor γ: Implications for Cardiovascular Disease", Hypertension, 43(2), pp.297~305 (2004), Ovid Technologies (Wolters Kluwer Health)[DOI]
- Malkeet S. Bahia, "Tumor Necrosis Factor Alpha Converting Enzyme: An Encouraging Target for Various Inflammatory Disorders", Chemical Biology & Drug Design, 75(5), pp.415~443 (2010), Wiley[DOI]
- Shirshendu DasGupta, "Current perspective of TACE inhibitors: A review", Bioorganic & Medicinal Chemistry, 17(2), pp.444~459 (2009), Elsevier BV[DOI]
- N. Bostanci, "Tumor Necrosis Factor-α-converting Enzyme (TACE) Levels in Periodontal Diseases", Journal of Dental Research, 87(3), pp.273~277 (2008), SAGE Publications[DOI]
- A. Monroy, "Impaired regulation of the TNF-α converting enzyme", tissue inhibitor of metalloproteinase 3 proteolytic system in skeletal muscle of obese type 2 diabetic patients: a new mechanism of insulin resistance in humans, 2009, pp.52(10), 2169~2181[DOI]
- Jotterand H, "Cathepsin D in the connective tissue and epithelium of inflammed human gingiva", J Biol Buccale, 5, pp.333~342 (1977)
- D. Feron, "Significant lower VVH7-like immunoreactivity serum level in diabetic patients: Evidence for independence from metabolic control and three key enzymes in hemorphin metabolism, cathepsin D, ACE and DPP-IV", Peptides, 30(2), pp.256~261 (2009), Elsevier BV[DOI]