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Nitric oxide production by hepatocytes contributes to the inhibitory effect of endotoxin on insulin-like growth factor I gene expression.
J Endocrinol. 2006 Sep; 190(3):847-56.JE

Abstract

We tested whether endotoxin (lipopolysaccharide, LPS) inhibits IGF-I gene expression in hepatocytes and the possible role of Kupffer cells and nitric oxide (NO) in this effect. LPS decreased IGF-I mRNA in hepatocyte cultures and increased the nitrite + nitrate levels in the culture medium. Furthermore, there was a negative correlation between the IGF-I mRNA and the nitrite+nitrate levels. When hepatocytes were cocultured with Kupffer cells, the inhibitory effect of LPS on IGF-I mRNA was higher than in hepatocyte cultures, but the stimulatory effect on nitrite+nitrate was similar in both conditions. The exogenous NO donated by S-nitroso-n-acetyl-d,l-penicillamide also decreased the IGF-I gene expression in hepatocyte cultures. In addition, two specific inducible NO synthase (iNOS) inhibitors, l-N6-(1-iminoethyl)lysine (l-NIL) and aminoguanidine, prevented the effect of LPS on nitrite+nitrate levels and on IGF-I gene expression in hepatocyte cultures. These data indicate that iNOS-derived NO may cause downregulation of IGF-I gene expression in hepatocytes. However, in cocultures, the iNOS inhibitor l-NIL prevented the effect of LPS on nitrite+nitrate levels, but only attenuated the LPS-induced decrease in IGF-I gene expression. We conclude that in hepatocytes, LPS-induced decrease in IGF-I is mainly due to induction of iNOS, whereas in the presence of Kupffer cells LPS inhibits IGF-I through NO release and through other inhibitory pathways.

Authors+Show Affiliations

Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17003285

Citation

Priego, Teresa, et al. "Nitric Oxide Production By Hepatocytes Contributes to the Inhibitory Effect of Endotoxin On Insulin-like Growth Factor I Gene Expression." The Journal of Endocrinology, vol. 190, no. 3, 2006, pp. 847-56.
Priego T, Granado M, Castillero E, et al. Nitric oxide production by hepatocytes contributes to the inhibitory effect of endotoxin on insulin-like growth factor I gene expression. J Endocrinol. 2006;190(3):847-56.
Priego, T., Granado, M., Castillero, E., Martín, A. I., Villanúa, M. A., & López-Calderón, A. (2006). Nitric oxide production by hepatocytes contributes to the inhibitory effect of endotoxin on insulin-like growth factor I gene expression. The Journal of Endocrinology, 190(3), 847-56.
Priego T, et al. Nitric Oxide Production By Hepatocytes Contributes to the Inhibitory Effect of Endotoxin On Insulin-like Growth Factor I Gene Expression. J Endocrinol. 2006;190(3):847-56. PubMed PMID: 17003285.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitric oxide production by hepatocytes contributes to the inhibitory effect of endotoxin on insulin-like growth factor I gene expression. AU - Priego,Teresa, AU - Granado,Miriam, AU - Castillero,Estibaliz, AU - Martín,Ana Isabel, AU - Villanúa,M Angeles, AU - López-Calderón,Asunción, PY - 2006/9/28/pubmed PY - 2006/12/19/medline PY - 2006/9/28/entrez SP - 847 EP - 56 JF - The Journal of endocrinology JO - J Endocrinol VL - 190 IS - 3 N2 - We tested whether endotoxin (lipopolysaccharide, LPS) inhibits IGF-I gene expression in hepatocytes and the possible role of Kupffer cells and nitric oxide (NO) in this effect. LPS decreased IGF-I mRNA in hepatocyte cultures and increased the nitrite + nitrate levels in the culture medium. Furthermore, there was a negative correlation between the IGF-I mRNA and the nitrite+nitrate levels. When hepatocytes were cocultured with Kupffer cells, the inhibitory effect of LPS on IGF-I mRNA was higher than in hepatocyte cultures, but the stimulatory effect on nitrite+nitrate was similar in both conditions. The exogenous NO donated by S-nitroso-n-acetyl-d,l-penicillamide also decreased the IGF-I gene expression in hepatocyte cultures. In addition, two specific inducible NO synthase (iNOS) inhibitors, l-N6-(1-iminoethyl)lysine (l-NIL) and aminoguanidine, prevented the effect of LPS on nitrite+nitrate levels and on IGF-I gene expression in hepatocyte cultures. These data indicate that iNOS-derived NO may cause downregulation of IGF-I gene expression in hepatocytes. However, in cocultures, the iNOS inhibitor l-NIL prevented the effect of LPS on nitrite+nitrate levels, but only attenuated the LPS-induced decrease in IGF-I gene expression. We conclude that in hepatocytes, LPS-induced decrease in IGF-I is mainly due to induction of iNOS, whereas in the presence of Kupffer cells LPS inhibits IGF-I through NO release and through other inhibitory pathways. SN - 0022-0795 UR - https://www.unboundmedicine.com/medline/citation/17003285/Nitric_oxide_production_by_hepatocytes_contributes_to_the_inhibitory_effect_of_endotoxin_on_insulin_like_growth_factor_I_gene_expression_ L2 - https://joe.bioscientifica.com/doi/10.1677/joe.1.06938 DB - PRIME DP - Unbound Medicine ER -