Interleukin-1β enhances retinoic acid-mediated expression of bone-type alkaline phosphatase in rat IEC-6 cells

Takeshi Nikawa, Madoka Ikemoto, Kaori Tokuoka, Shigetada Teshima, David H. Alpers, Yoshihiro Masui, Kyoichi Kishi, Kazuhito Rokutan

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

We previously showed that vitamin A upregulated the expression of bone-type alkaline phosphatase (ALP) in fetal rat small intestine and rat intestinal IEC-6 cells. In this study, we examined interactions between retinoic acid (RA) and several growth factors/cytokines on the isozyme expression in IEC-6 cells. Epidermal growth factor and interleukins (ILs)-2, -4, -5, and -6 completely blocked the RA-mediated increase in ALP activity. In contrast, IL-1β markedly increased the activity, protein, and mRNA of the bone-type ALP only when RA was present. IL-1β and/or RA did not change the type 1 IL-1 receptor transcript level, whereas IL-1β enhanced the RA-induced expressions of retinoic acid receptor-β (RAR-β) and retinoid X receptor-β (RXR-β) mRNAs and RA-mediated RXR response element binding. The synergism of IL-1β and RA on ALP activity was completely blocked by protein kinase C (PKC) inhibitors. Our results suggest that IL-1β may modify the ALP isozyme expression in small intestinal epithelial cells by stimulating PKC-dependent, RAR-β- and/or RXR-βmediated signaling pathways.

Original languageEnglish
Pages (from-to)G510-G517
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume280
Issue number3 43-3
StatePublished - Mar 1 2001

Keywords

  • Alkaline phosphatase isozymes
  • Fetal rat small intestine
  • Protein kinase C
  • Retinoic acid receptors
  • Retinoid X receptors

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