Genes profile related to modulation of natural killer cell activity induced by electroacupuncture

전침이 자연살해세포 활성에 미치는 유전자 발현 profile에 대한 연구

  • Choi, Gi-soon (Department of East-West Medicine, Graduate School, Kyung-Hee University) ;
  • No, Sam-woong (Department of Physiology, College of Oriental Medicine, Kyung-Hee University) ;
  • Oh, Sang-deog (Department of East-West Medicine, Graduate School, Kyung-Hee University) ;
  • Bae, Hyun-su (Department of Physiology, College of Oriental Medicine, Kyung-Hee University) ;
  • Ahn, Hyun-jong (Department of Microbiology, College of Medicine, Kyung-Hee University) ;
  • Ha, Yoon-mun (Department of Microbiology, College of Medicine, Kyung-Hee University) ;
  • Kim, Kwang-ho (Department of Preventive Medicine, College of Oriental Medicine, Kyung-Hee University) ;
  • Min, Byung-il (Department of East-West Medicine, Graduate School, Kyung-Hee University)
  • 최기순 (경희대학교 대학원 동서의학과) ;
  • 노삼웅 (경희대학교 한의과대학 생리학교실) ;
  • 오상덕 (경희대학교 대학원 동서의학과) ;
  • 배현수 (경희대학교 한의과대학 생리학교실) ;
  • 안현종 (경희대학교 의과대학 미생물학교실) ;
  • 하윤문 (경희대학교 의과대학 미생물학교실) ;
  • 김강호 (경희대학교 한의과대학 예방의학교실) ;
  • 민병일 (경희대학교 대학원 동서의학과)
  • Received : 2002.10.14
  • Accepted : 2002.11.23
  • Published : 2002.12.20

Abstract

A line of study reported that electroacupuncture(EA) modulate natural killer cell(NK Cell) activities. One report suggested that EA enhanced splenic interferon-gamma($IFN-{\gamma}$), interleukin-2(IL-2), and NK cell activity in Sprague-Dawley rats. Another study suggested that $IFN-{\gamma}$ mediates the up-regulation of NK cell activity, and endogenous ${\beta}$-endorphin secretion also play a role in the up-regulation of NK cell activity induced by EA stimulation. In order to better understand the molecular regulation underlying the activation of NK cell induced by EA, we have utilized cDNA microarray to elucidate how EA alters program of gene expression of spleen in rats. First, we divided three groups, group I was EA group treated with EA in restriction holder, group II was sham group with only holder stress, and last group III was control group with no treatment. We measured NK cell activity after EA stimulation three times for 2 days using $^{51}Cr$ release assay. Second, Biotin-labeled cDNA probes synthesized from EA group and sham group, were competitively hybridized to the microarray that contained variable genes. Such high-throughput screening has identified a number of EA-responsive gene candidates. Of these, we found that EA induced a subset of genes of genes that functionally could modulatory effects on NK cell activity. Genes(vascular cell adhesion molecule-1, protein-tyrosine kinase, CD94 mRNA) related to boost NK cell activity, were increased by EA And, genes(protein-tyrosine-phospatase mRNA, protein-tyrosine phosphatase(SHP-1) mRNA) related to inhibit NK cell activity, were decreased by EA. These EA-responsive genes may provide key insights from which to understand mechanisms of activation of NK cell induced by EA.

Keywords

Acknowledgement

Supported by : 한국과학재단