Gene Expression Profile in Carpal Tunnel Syndrome Patients

  • Kim, Hye-Won (Department of Biochemistry & Molecular biology, Korea University Medical College) ;
  • Kim, Ki-Nam (Department of Biochemistry & Molecular biology, Korea University Medical College) ;
  • Seo, Sang-Hui (Department of Biochemistry & Molecular biology, Korea University Medical College) ;
  • Lee, Seung-Ho (Department of Biochemistry & Molecular biology, Korea University Medical College) ;
  • Sohn, Sung-Hwa (Department of Biochemistry & Molecular biology, Korea University Medical College) ;
  • Kim, Yu-Ri (Department of Biochemistry & Molecular biology, Korea University Medical College) ;
  • HaLee, Young-Mie (Research Institute of basic sciences, College of literature and science, Yonsei University) ;
  • Shim, Jae-Sun (Division of Plastic and Reconstructive Surgery, Korean University) ;
  • Ahn, Duck-Sun (Division of Plastic and Reconstructive Surgery, Korean University) ;
  • Kim, Meyoung-Kon (Department of Biochemistry & Molecular biology, Korea University Medical College)
  • 발행 : 2006.12.31

초록

Carpal tunnel syndrome (CTS) is one of the most common disorders by under pressure of the median nerve at the wrist in these days. However, pathological mechanism of CTS is unknown. We carried out this study to identify the changes of gene expression and to evaluate possible mechanism in CTS. 120 CTS patients and 30 control patients were included in this study. Patients with a history of diabetes, hypertension, thyroid diseases, and arthritis were excluded. CTS patients were divided to three experimental groups-Mild, Moderate, and Severe group-according to elecrodiagnosis. Radioactive cDNA microarrays (Nylon membrane including 1,152 genes) were used to examine the difference of gene expression profile in CTS. We identified up-regulated genes by more than 2.0 value of z-ratio, and down-regulated genes by less than-2.0 value of z-ratio. 20 genes such as the ITGAL, ITGAM, PECAM1, VIL2, TGFBR2, RAB7, RNF5 and NFKB1 were up-regulated, and 28 genes such as PRG5, CASP8, CDH1, IGFBP5, CBX3, HREV107, PIN, and WINT2 were down-regulated. These genes were related with TGF beta signaling pathway, NF-Kb signaling pathway, antiapoptotic pathway and T cell receptor signaling pathway. However, there were no differences in gene expression profiles according to severities of symptoms. We suggest that CTS could be related with proinflammatory mechanism and antiapoptotic mechanism.

키워드

참고문헌

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