Altered gene expression in leukocyte transendothelial migration and cell communication pathways in periodontitis-affected gingival tissues

Abe D, Kubota T, Morozumi T, Shimizu T, Nakasone N, Itagaki M, Yoshie H. Altered gene expression in leukocyte transendothelial migration and cell communication pathways in periodontitis‐affected gingival tissues. J Periodont Res 2011; 46: 345–353. © 2011 John Wiley & Sons A/S Background and Obje...

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Published in:Journal of periodontal research 2011-06, Vol.46 (3), p.345-353
Main Authors: Abe, D., Kubota, T., Morozumi, T., Shimizu, T., Nakasone, N., Itagaki, M., Yoshie, H.
Format: Article
Language:English
Subjects:
Adult
Biological and medical sciences
CD18 Antigens - genetics
Cell Communication - immunology
Chemokine CXCL12 - genetics
Chemotaxis, Leukocyte - immunology
Chronic Periodontitis - immunology
Chronic Periodontitis - pathology
Connexins - genetics
Desmocollins - genetics
Desmoglein 1 - genetics
DNA microarray
Down-Regulation - genetics
Endothelial Cells - immunology
Endothelial Cells - pathology
Facial bones, jaws, teeth, parodontium: diseases, semeiology
Female
gene expression
Gene Expression - genetics
Gene Expression Regulation - genetics
Gingiva - immunology
Gingiva - pathology
Humans
Indexing in process
Intermediate Filament Proteins - genetics
Leukocytes - immunology
Male
Matrix Metalloproteinase 2 - genetics
Medical sciences
Microarray Analysis
Middle Aged
Nerve Tissue Proteins - genetics
Nestin
Non tumoral diseases
Otorhinolaryngology. Stomatology
pathogenesis of periodontal diseases
periodontitis
rac GTP-Binding Proteins - genetics
RAC2 GTP-Binding Protein
Receptors, CXCR4 - genetics
Reverse Transcriptase Polymerase Chain Reaction
RNA - genetics
Transendothelial and Transepithelial Migration - immunology
Up-Regulation - genetics
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Summary:Abe D, Kubota T, Morozumi T, Shimizu T, Nakasone N, Itagaki M, Yoshie H. Altered gene expression in leukocyte transendothelial migration and cell communication pathways in periodontitis‐affected gingival tissues. J Periodont Res 2011; 46: 345–353. © 2011 John Wiley & Sons A/S Background and Objective:  Gene expression is related to the pathogenesis of periodontitis and plays a crucial role in local tissue destruction and disease susceptibility. The aims of the present study were to identify the expression of specific genes and biological pathways in periodontitis‐affected gingival tissue using microarray and quantitative real‐time RT‐PCR analyses. Material and Methods:  Healthy and periodontitis‐affected gingival tissues were taken from three patients with severe chronic periodontitis. Total RNAs from six gingival tissue samples were used for microarray analyses. Data‐mining analyses, such as comparisons, gene ontology and pathway analyses, were performed and biological pathways with a significant role in periodontitis were identified. In addition, quantitative real‐time RT‐PCR analysis was performed on samples obtained from 14 patients with chronic periodontitis and from 14 healthy individuals in order to confirm the results of the pathway analysis. Results:  Comparison analyses found 15 up‐regulated and 13 down‐regulated genes (all of which showed a change of more than twofold in expression levels) in periodontitis‐affected gingival tissues. Pathway analysis identified 15 up‐regulated biological pathways, including leukocyte transendothelial migration, and five down‐regulated pathways, including cell communication. Quantitative real‐time RT‐PCR verified that five genes in the leukocyte transendothelial migration pathway were significantly up‐regulated, and four genes in the cell communication pathway were significantly down‐regulated, which was consistent with pathway analysis. Conclusion:  We identified up‐regulated genes (ITGB‐2, MMP‐2, CXCL‐12, CXCR‐4 and Rac‐2) and down‐regulated genes (connexin, DSG‐1, DSC‐1 and nestin) in periodontitis‐affected gingival tissues; these genes may be related to the stimulation of leukocyte transendothelial migration and to the the impairment of cell‐to‐cell communication in periodontitis.
ISSN:0022-3484
1600-0765
DOI:10.1111/j.1600-0765.2011.01349.x