- AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
We previously reported that interleukin-l (IL-1) promoted the survival of murine osteoclast-like cells (OCLs) formed in vitro and activated a transcription factor, NF-kappa B, of OCLs. The present study examined whether the activation of NF-kappa B is directly involved in the survival of OCLs promoted by IL-1. The expression of IL-l 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-l transiently activated NP-kappa B in the nuclei of the OCLs, and the maximal activation occurred at 30 min. The degradation of I kappa B alpha coincided with the activation of NF-kappa B in the OCLs. The immunocytochemical study revealed that p65, a subunit of NF-kappa B, was translocated from the cytoplasm into almost all of the nuclei of the OCLs within 30 min after IL-I stimulation. The purified OCLs spontaneously died via apoptosis, and IL-l 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-kappa B and prevented the survival of OCLs supported by IL-1. When OCLs were pretreated with antisense oligodeoxynucleotides to p65 and p50 of NF-kappa B, the expression of respective mRNAs by OCLs was suppressed, and the IL-l-induced survival of OCLs was concomitantly inhibited. These results indicate that IL-1 promotes the survival of osteoclasts through the activation of NF-kappa B.
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