Interleukin‐1β刺激ヒト顎関節滑膜細胞のGeneChip遺伝子発現プロファイリング―Interleukin‐1とそのレセプター,ケモカインの発現について―

  • 小倉 直美
    日本大学松戸歯学部顎顔面外科学講座 日本大学松戸歯学部口腔科学研究所
  • 戸邊 真希子
    日本大学松戸歯学部顎顔面外科学講座
  • 酒巻 裕之
    日本大学松戸歯学部顎顔面外科学講座 日本大学松戸歯学部口腔科学研究所
  • 秋葉 正一
    総合病院国保旭中央病院歯科口腔外科
  • 安孫子 宜光
    日本大学松戸歯学部生化学・分子生物学講座 日本大学松戸歯学部口腔科学研究所
  • 近藤 壽郎
    日本大学松戸歯学部顎顔面外科学講座 日本大学松戸歯学部口腔科学研究所

書誌事項

タイトル別名
  • Gene expression profiling of interleukin-1.BETA.-stimulated synovial fibroblasts from TMJ using GeneChip-Expressions of interleukin-1, its receptor, and chemokines-
  • Interleukin 1 ベータ シゲキ ヒト ガク カンセツカツマク サイボウ ノ GeneChip イデンシ ハツゲン プロファイリング Interleukin 1 ト ソノ レセプター ケモカイン ノ ハツゲン ニ ツイテ
  • Expressions of interleukin-1, its receptor, and chemokines
  • Interleukin-1とそのレセプター, ケモカインの発現について

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抄録

Interleukin (IL)-1β responsible gene expressions in sy novialcells obtained from the human temporomandibular joint (TMJ) were analyzed using GeneChips. Synovial cells (TMJ1 and TMJ2) were obtained from synovial tis sueof two patients who underwent arthrotomy of TMJ using a method of out-growth. The synovial cells were stimulated with IL-1β for 4 hours, and then total RNA was extracted using RNeasy kit. Gene expression profil ingwas analyzed using the Affymetrix Human Genome Focus Array. The analysis of the hybridization data was performed using GeneSpring software. TMJ1 and TMJ2 expressed vimentin, prolyl 4-hydroxylase and type I col lagen, which are markers for fibroblasts. In contrast, the expression of HLA class II antigens were not detected. Among 8, 763 genes in the microarray, 192 genes, 154 up regulatedand 38 down-regulated genes, showed intensity greater than a 2-fold difference between with and with outIL-1β-treatment in both of TMJ1 and TMJ2. The genes whose levels were significantly altered by IL-1β could be classified into categories of enzyme and signal transducer. TMJ1 and TMJ2 constitutively express genes of IL-1 receptor type I and its associated mol ecules.Gene expression of IL-1β was stimulated by IL-1β. In contrast, IL-1α gene expression was not detected. The most significantly up-regulated gene was CCL20 (MIP-3α), which is a member of the chemokine super family. Gene expression of 12 chemokines was increased more than 2-fold by IL-1, 3-treatment in both of TMJ1 and TMJ2. In conclusion, IL-1β may cause abnormalities associated with intracapsular pathologic conditions of the TMJ through enhancement of gene expression for IL-1β and chemokines in synovial cells.

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