Transcriptomes in healthy and diseased gingival tissues.
Transcriptomes in healthy and diseased gingival tissues.
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DOI:
10.1902/jop.2008.080139
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发表时间:
2008-11
影响因子:
4.3
通讯作者:
Papapanou PN
中科院分区:
文献类型:
--
作者:
Demmer RT;Behle JH;Wolf DL;Handfield M;Kebschull M;Celenti R;Pavlidis P;Papapanou PN
Clinical and radiographic measures are gold standards for diagnosing periodontitis but offer little information regarding the pathogenesis of the disease. We hypothesized that a comparison of gene expression signatures between healthy and diseased gingival tissues would provide novel insights in the pathobiology of periodontitis, and would inform the design of future studies. Ninety systemically healthy non-smokers with moderate to advanced periodontitis (63 with chronic and 27 with aggressive periodontitis) each contributed with ≥2 “diseased” interproximal papillae [with bleeding on probing (BoP), pocket depth (PD) ≥4mm, and attachment loss (AL) ≥3mm)] and a “healthy” papilla, if available (no BoP, PD ≤4mm and AL ≤2mm). RNA was extracted, amplified, reverse-transcribed, labeled, and hybridized with AffymetrixU133Plus2.0 arrays. Differential expression was assayed in 247 individual tissue samples (183 from diseased and 64 from healthy sites) using a standard mixed-effects linear model approach, with patient effects considered random with a normal distribution, and gingival tissue status considered a two-level fixed effect. Gene ontology analysis summarized the expression patterns into biologically relevant categories. Transcriptome analysis revealed that a total of 12,744 probe sets were differentially expressed after adjusting for multiple comparisons (p<9.15×10-7). Of those, 5,295 were up-regulated and 7,449 down-regulated in disease when compared to health. Gene ontology analysis identified 61 differentially expressed groups (adjusted p<0.05) including apoptosis, antimicrobial humoral response, antigen presentation, regulation of metabolic processes, signal transduction, and angiogenesis. Gingival tissue transcriptomes provide a valuable scientific tool for further hypothesis-driven studies of the pathobiology of periodontitis.
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影响因子:
14.9
作者:
Khatri P;Voichita C;Kattan K;Ansari N;Khatri A;Georgescu C;Tarca AL;Draghici S
通讯作者:
Draghici S
影响因子:
4.3
作者:
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通讯作者:
Yoshie, Hiromasa
影响因子:
3.4
作者:
Handfield, M;Mans, JJ;Lamont, RJ
通讯作者:
Lamont, RJ
DOI:
10.1016/s0736-5748(02)00041-2
发表时间:
2002-06-01
影响因子:
1.8
作者:
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通讯作者:
Kunkel, LM
影响因子:
6.7
作者:
LISTGARTEN, MA;HELLDEN, L
通讯作者:
HELLDEN, L