Induction of cytokine-induced neutrophil chemoattractant in response to various stresses in rat C6 glioma cells

Takashi Uehara, Itsuko Baba, Yasuyuki Nomura

研究成果査読

22 被引用数 (Scopus)

抄録

The effect of stress on the production of cytokine-induced neutrophil chemoattractant (CINC) was examined in rat C6 glioma cells. We studied the production of CINC, an inteleukin-8 (IL-8) family protein, with bacterial endotoxin, H2O2, and tumor necrosis factor-α (TNF-α). Each stress induced CINC mRNA in a concentration-dependent manner. Since stress activates the protein kinases regulating nuclear transcription factors, we examined the effects of protein kinase inhibitors and the over-expression of dominant- negative Ras on CINC mRNA expression. Neither over-expression of dominant- negative Ras nor pretreatment with PD98059 (MEK-1 inhibitor), SB203580 (p38MAPK inhibitor), or GF109203X (protein kinase C (PKC) inhibitor) altered stress-induced CINC mRNA expression. This suggests that the Ras-MAPK, p38MAPK, and PKC pathways are not involved in CINC mRNA expression in glial cells. On the other hand, pretreatment with herbimycin A, a potent tyrosine kinase inhibitor, or Ro31-8220, a non-selective serine/threonine kinase inhibitor, suppressed stress-induced CINC mRNA expression. This indicates that stress-induced CINC mRNA expression is mediated by herbimycin A-, or Ro31-8220-sensitive kinases in glial cells. Since stress activates NF-κB and NF-IL6, we examined that the effect of herbimycin A, which suppresses CINC mRNA expression, on NF-κB and NF-IL6 activation. Herbimycin A suppressed NF- κB but not NF-IL6. These results suggest that in rat glial cells, the factors that induce CINC mRNA expression are mediated by herbimycin A- sensitive NF-κB activation, but not through the PKC, Ras-MAPK or p38 MAPK pathways.

本文言語English
ページ(範囲)284-292
ページ数9
ジャーナルBrain Research
790
1-2
DOI
出版ステータスPublished - 4月 20 1998
外部発表はい

ASJC Scopus subject areas

  • 神経科学一般
  • 分子生物学
  • 臨床神経学
  • 発生生物学

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