Activation of NF-κB is involved in the survival of osteoclasts promoted by interleukin-1

Eijiro Jimi, Ichiro Nakamura, Tetsuro Ikebe, Shuichi Akiyama, Naoyuki Takahashi, Tatsuo Suda

研究成果: ジャーナルへの寄稿学術誌査読

173 被引用数 (Scopus)

抄録

We previously reported that interleukin-1 (IL-1) promoted the survival of murine osteoclast-like cells (OCLs) formed in vitro and activated a transcription factor, NF-κB, of OCLs. The present study examined whether the activation of NF-κB is directly involved in the survival of OCLs promoted by IL-1. The expression of IL-1 type I receptor mRNA in OCLs was detected by the polymerase chain reaction amplification of reverse-transcribed mRNA. An electrophoretic mobility shift assay showed that IL-1 transiently activated NF-κB in the nuclei of the OCLs, and the maximal activation occurred at 30 min. The degradation of IκBα coincided with the activation of NF-κB in the OCLs. The immunocytochemical study revealed that p65, a subunit of NF-κB, was translocated cytoplasm into almost almost of the nuclei of the OCLs within 30 min after IL-1 stimulation. The purified OCLs spontaneously died via apoptosis, and IL-1 promoted the Survival of OCLs by preventing their apoptosis. The pretreatment of purified OCLs with proteasome inhibitors suppressed the IL-1-induced activation of NF-κB and prevented the survival of OCLs supported by IL-1. When OCLs were pretreated with antisense oligodeoxynucleotides to p65 and p50 of NF-κB, the expression of respective mRNAs by OCLs was suppressed, and the IL-1-induced survival of OCLs was concomitantly inhibited. These results indicate that IL-1 promotes the survival of osteoclasts through the activation of NF-κB.

本文言語英語
ページ(範囲)8799-8805
ページ数7
ジャーナルJournal of Biological Chemistry
273
15
DOI
出版ステータス出版済み - 4月 10 1998
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 生化学
  • 分子生物学
  • 細胞生物学

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