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  • Title: Modulation of complement component (C3 and factor B) biosynthesis by a histone deacetylase inhibitor in human intestinal epithelial cells.
    Author: Andoh A, Fujiyama Y, Shimada M, Bamba T.
    Journal: Int J Mol Med; 2000 Jul; 6(1):51-4. PubMed ID: 10851266.
    Abstract:
    Sodium butyrate enhances TNF-alpha-induced complement C3 secretion but suppresses TNF-alpha-induced factor B secretion in intestinal epithelial cells. To further evaluate the mechanism underlying these responses, we assessed the effects of trichostatin A, a compound structurally unrelated to butyrate and a potent inhibitor of histone deacetylase. The C3 and factor B secretion was evaluated by enzyme-linked immunosorbent assay (ELISA) and Northern blot, and the activation of transcription factor was assessed by an electrophoretic gel mobility shift assay (EMSA). Like sodium butyrate, trichostatin A enhanced TNF-alpha-induced C3 secretion, but suppressed TNF-alpha-induced factor B secretion. These effects were also observed at the level of mRNA. EMSAs indicated that trichostatin A weakly suppressed TNF-alpha-induced NF-kappaB and NF-IL6 activation. These observations differ from previous reports that sodium butyrate potently suppressed NF-kappaB activation but enhanced NF-IL6 activation. Trichostatin A modulated TNF-alpha-induced C3 and factor B secretion in a manner similar to that induced by sodium butyrate, suggesting that both sodium butyrate and trichostatin A exert certain counter-regulatory effects associated with histone hyperacetylation. However, it remains to be determined which factors other than histone acetylation are responsible for the counter-regulation of TNF-alpha-induced C3 and factor B gene expression.
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