TY - JOUR
T1 - Interleukin-1β enhances retinoic acid-mediated expression of bone-type alkaline phosphatase in rat IEC-6 cells
AU - Nikawa, Takeshi
AU - Ikemoto, Madoka
AU - Tokuoka, Kaori
AU - Teshima, Shigetada
AU - Alpers, David H.
AU - Masui, Yoshihiro
AU - Kishi, Kyoichi
AU - Rokutan, Kazuhito
PY - 2001/3
Y1 - 2001/3
N2 - 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.
AB - 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.
KW - Alkaline phosphatase isozymes
KW - Fetal rat small intestine
KW - Protein kinase C
KW - Retinoic acid receptors
KW - Retinoid X receptors
UR - http://www.scopus.com/inward/record.url?scp=0035000306&partnerID=8YFLogxK
U2 - 10.1152/ajpgi.2001.280.3.g510
DO - 10.1152/ajpgi.2001.280.3.g510
M3 - Article
C2 - 11171635
AN - SCOPUS:0035000306
SN - 0193-1857
VL - 280
SP - G510-G517
JO - American Journal of Physiology - Gastrointestinal and Liver Physiology
JF - American Journal of Physiology - Gastrointestinal and Liver Physiology
IS - 3 43-3
ER -