Korean Journal of Veterinary Research (대한수의학회지)

The Korean Society of Veterinary Science (대한수의학회)
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Extracellular signal regulated kinases in the spinal cord of rats with experimental autoimmune encephalomyelitis

자기면역성 뇌척수염 조직에서 extracellular signal regulated kinases의 발현

  • Ahn, Mee-jung (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University) ;
  • Heo, Seung-dam (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University) ;
  • Jee, Young-heun (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University) ;
  • Joo, Hong-gu (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University) ;
  • Lee, Yong-duk (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University) ;
  • Sim, Ki-Bum (Department of Neurosurgery, College of Medicine, Cheju National University) ;
  • Shin, Tae-kyun (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
  • 안미정 (제주대학교 농업생명과학대학 수의학과) ;
  • 허승담 (제주대학교 농업생명과학대학 수의학과) ;
  • 지영흔 (제주대학교 농업생명과학대학 수의학과) ;
  • 주홍구 (제주대학교 농업생명과학대학 수의학과) ;
  • 이용덕 (제주대학교 농업생명과학대학 수의학과) ;
  • 심기범 (제주대학교 의과대학 신경외과학교실) ;
  • 신태균 (제주대학교 농업생명과학대학 수의학과)
  • Accepted : 2003.12.01
  • Published : 2003.12.25
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Abstract

The phosphorylation of extracellular signal-regulated kinases (p-ERK) in the spinal cord of rats with acute monophasic experimental autoimmune encephalomyelitis (EAE) was studied using immunohistochemistry and treatment with inhibitor. P-ERK is constitutively expressed in glial cells in the normal spinal cord. In EAE, some inflammatory cells in the subarachnoid space were positive for p-ERK at the early stage, and its immunoreactivity declined when those cells infiltrated the parenchyma at the peak stage. In a blocking experiment using its inhibitor, the intravenous administration of PD98059 from day 7 to 13 post-immunization did not modulate EAE paralysis. Considering the results, we postulate that intravenous administration of PD98059 is not effective in ameliorating EAE paralysis, although many inflammatory cells express ERK in the subarachnoid space.

Keywords

References

  1. Aikawa, R., Komuro, I., Yamazaki, T., Zou, Y., Kudoh, S., Tanaka, M., Shiojima, I., Hiroi, Y. and Yazaki, Y. Oxidative stress activates extracellular signal-regulated kinases through Src and Ras in cultured cardiac myocytes of neonatal rats. J Clin Invest. 1997, 100, 1813-1821
  2. Boulton, T. G., Nye, S. H., Robbins, D. J., IP, N. Y., Radziejewska, E., Morgenbesser, S. D., DePinho, R. A., Panayotatos, N., Cobb, M. H. and Yancopoulos, G. D. ERKs: a family of protein-serine/threonine kinases that are activated and tyrosine phosphorylated in response to insulin and NGF. Cell. 1991, 65, 663-675
  3. Bonvin, C., Guillon, A., van Bemmelen, M. X., Gerwins, P., Johnson, G. L. and Widmann, C. Role of the amino-terminal domains of MEKKs in the activation of NF kappa B and MAPK pathways and in the regulation of cell proliferation and apoptosis. Cell Signal. 2002, 14, 123-131
  4. Chang, L. and Karin, M. K. Mammalian MAP kinase signalling cascades. Nature, 2001, 410, 37-40
  5. Fung, M. M., Rohwer, F. and McGuire, K. L. IL-2 activation of a PI3K-dependent STAT3 serine phosphorylation pathway in primary human T cells. Cell Signal. 2003, 15(6), 625-636
  6. Garrington, T. P. and Johnson, G. L. Organization and regulation of mitogen-activated protein kinase signaling pathways. Curr. Opin. Cell Biol. 1999, 11, 211-218
  7. Johnson, G. L. and Lapadat. R. Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science, 2002, 298, 1911-1912
  8. Mori, T., Wang, X., Jung, J. C., Sumii, T, Singhal, A. B., Fini, M. E., Dixon, C. E., Alessandrini, A. and Lo, E. H. Mitogen-activated protein kinase inhibition in traumatic brain injury: in vitro and in vivo effects. J. Cerebr. Blood Flow Metab, 2002, 22, 444-452
  9. Namura, S., Iihara, K., Takami, S., Nagata, I., Kikuchi, H., Matsushita, K., Moskowitz, M. A., Bonventre, J. V. and Alessandrini, A. Intravenous administration of MEK inhibitor U0126 affords brain protection against forebrain ischemia and focal cerebral ischemia. Proc. Natl. Acad. Sci. U.S.A. 2001, 98, 11569-11574
  10. Otani, N., Nawashiro, H., Fukui, S., Nomura, N., Yano, A., Miyazawa, T. and Shima, K. Differential activation of mitogen-activated protein kinase pathways after traumatic brain injury in the rat hippocampus. J. Cereb. Blood Flow Metab. 2002, 22, 327-334
  11. Shin, T., Kojima, T., Tanuma, N.. Ishihara, Y. and Matsumoto, Y. The subarachnoid space as a site for precursor T cell proliferation and effector T cell selection in experimental autoimmune encephalomyelitis. J. Neuroimmunol. 1995, 56, 171-178
  12. Shin, T., Ahn, M., Jung, K., Heo, S., Kim, D., Jee, Y., Lim, Y. K. and Yeo, E. J. Activation of mitogen-activated protein kinases in experimental autoimmune encephalomyelitis. J. Neuroimmunol. 2003, 140, 118-125