Regulation of haptoglobin gene expression in 3T3-L1 adipocytes by cytokines, catecholamines, and PPAR gamma

Regulation of haptoglobin gene expression in 3T3-L1 adipocytes by cytokines, catecholamines, and PPAR gamma

Autor Nascimento, C. O. do Google Scholar
Hunter, L. Google Scholar
Trayhurn, P. Google Scholar
Instituição Univ Liverpool
Universidade Federal de São Paulo (UNIFESP)
Resumo Factors which regulate expression of the haptoglobin (acute phase reactant) gene in adipocytes have been examined using 3T3-L1 cells. Haptoglobin expression was observed by Northern blotting in each of the major white adipose tissue depots of mice (epididymal, subcutaneous, mesenteric, and perirenal) and in interscapular brown fat. Expression occurred in mature adipocytes, but not in the stromal-vascular fraction. in 3T3-L1 cells, haptoglobin mRNA was detected from day 4 after the induction of differentiation into adipocytes. Lipopolysaccharide and the cytokines, TNFalpha and interleukin-6, resulted in substantial increases in haptoglobin mRNA in 3T3-L1 adipocytes; the increase (7-fold) was highest with TNFalpha. Increases in haptoglobin mRNA level were also induced by dexamethasone, noradrenaline, isoprenaline, and a beta3-adrenoceptor agonist. in contrast, haptoglobin mRNA was reduced by nicotinic acid and the PPARgamma agonist, rosiglitazone. RT-PCR showed that the haptoglobin gene was expressed in human adipose tissue (subcutaneous, omental). It is concluded that haptoglobin gene expression in adipocytes is stimulated by inflammatory cytokines, glucocorticoids, and the sympathetic system, while activation of the PPARgamma nuclear receptor is strongly inhibitory. (C) 2003 Elsevier Inc. All rights reserved.
Assunto acute phase reactant
gene expression
sympathetic nervous system
white adipose tissue
3T3-L1 cells
Idioma Inglês
Data 2004-01-16
Publicado em Biochemical and Biophysical Research Communications. San Diego: Academic Press Inc Elsevier Science, v. 313, n. 3, p. 702-708, 2004.
ISSN 0006-291X (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 702-708
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000187894400038

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