In vivo activation of the interleukin-6 receptor/gp130 signaling pathway in pituitary corticotropes of lipopolysaccharide-treated rats
Neuroendocrinology. 2003-01-01; 77(1): 32-43
DOI: 10.1159/000068336
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1. Neuroendocrinology. 2003 Jan;77(1):32-43.
In vivo activation of the interleukin-6 receptor/gp130 signaling pathway in
pituitary corticotropes of lipopolysaccharide-treated rats.
Gautron L(1), Lafon P, Tramu G, Layé S.
Author information:
(1)Laboratoire des Régulations Neuroendocriniennes, EA 2972, Université Bordeaux
I, Talence, France.
Adrenocorticotropic hormone (ACTH) release from anterior pituitary corticotropes
is greatly increased during peripheral inflammation induced by lipopolysaccharide
(LPS) administration. Interleukin-6 (IL-6) is thought to participate in
LPS-induced ACTH release, but whether or not corticotropes are directly targeted
by this cytokine is unclear. Therefore, we investigated the expression and
activation of IL-6 signaling components in the pituitary of rats 2 and 4 h after
administration of LPS (250 microg/kg). Intraperitoneal LPS treatment provoked the
nuclear translocation of signal transducer and activator of transcription 3
(STAT-3) and Fos expression in the anterior pituitary lobe, as demonstrated by
immunohistochemistry. By using in situ hybridization, we demonstrated that
suppressor of cytokine signaling 3 (SOCS-3) and c-fos mRNAs were significantly
induced by the LPS treatment in the anterior lobe of the pituitary. Dual in situ
hybridization revealed that most corticotropes expressed IL-6 receptor and gp130
mRNAs, and that 2 h after LPS treatment, SOCS-3 and c-fos mRNAs were induced in
corticotropes. Our results suggest that LPS-induced IL-6 could regulate the
hypothalamo-pituitary-adrenal axis by directly targeting corticotropes during
peripheral inflammation.
Copyright 2003 S. Karger AG, Basel
DOI: 10.1159/000068336
PMID: 12624539 [Indexed for MEDLINE]