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Interleukin-1 beta suppresses growth hormone-induced acid-labile subunit mRNA levels and secretion in primary hepatocytes.

Authors: Delhanty, P J 
Citation: Delhanty PJ, Biochem Biophys Res Commun. 1998 Feb 4;243(1):269-72.
Pubmed: (View Article at PubMed) PMID:9473516
DOI: Full-text: DOI:10.1006/bbrc.1998.8089

Cytokines are thought to mediate the catabolic states induced by infection and trauma. Recent evidence suggests that the cytokine interleukin-1 beta (IL-1 beta) directly inhibits the anabolic insulin-like growth factor (IGF)-I: growth hormone (GH) axis. The biological activity of circulating IGF is regulated by the hepatocyte derived, GH-dependent acid-labile subunit (ALS) of the 140-kDa IGF binding protein (IGFBP) complex. ALS buffers the growth and metabolic effects of the insulin-like growth factors by sequestering them in a ternary complex with IGFBP-3. To determine whether IL-1 beta has a direct effect on hepatic ALS production, we have examined its effect on ALS mRNA levels and secretion in hepatocytes under GH-induced and basal conditions. In the presence of GH (30 ng/mL) half-maximal reduction of ALS mRNA levels and secretion was induced by between 0.3-3 ng/mL rhIL-1 beta (P < 0.05). However, under basal conditions IL-1 beta had no significant effect on ALS mRNA levels, and only a slight suppression of secretion. Our study suggests that IL-1 beta regulates ALS gene expression and secretion in a way that is dependent, in part, on interaction with the GH signalling pathway.

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CRRD Object Information
CRRD ID: 12910942
Created: 2017-06-28
Species: All species
Last Modified: 2017-06-28
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.