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Cortisol stimulates growth hormone gene expression in rainbow trout leucocytes in vitro.

Authors :
Yada T
Muto K
Azuma T
Hyodo S
Schreck CB
Source :
General and comparative endocrinology [Gen Comp Endocrinol] 2005 May 15; Vol. 142 (1-2), pp. 248-55. Date of Electronic Publication: 2005 Feb 17.
Publication Year :
2005

Abstract

Extrapituitary expression of the growth hormone (GH) gene has been reported for the immune system of various vertebrates. In the rainbow trout (Oncorhynchus mykiss), GH mRNA could be detected in several lymphoid organs and leucocytes by reverse transcriptase-polymerase chain reaction (RT-PCR). To understand the control of GH expression in the fish immune system, mRNA levels for two distinct GH genes (GH1 and GH2) in trout leucocytes isolated from peripheral blood were quantified using a real-time PCR method. Both GH mRNAs could be detected in trout leucocytes, although their levels were extremely low compared to those in pituitary cells. The levels of GH2 mRNA in leucocytes were several times higher than those of GH1, while no difference was observed between GH1 and GH2 mRNA levels in the pituitary. Administration of dibutyryl cyclic AMP and cortisol produced a significant elevation of GH mRNA levels in trout leucocytes, although the levels were unchanged by T3. GH1 and GH2 mRNA levels showed similarities in responses to those factors. The effect of cortisol on GH mRNA appears biphasic; a dose-depending elevation of GH gene expression was observed in leucocytes treated with cortisol at below 200 nM, however, cortisol had no effect at 2000 nM. Cortisol-treated leucocytes showed no significant change in the mRNA level of beta-actin or proliferative activity during the experiments. Our results thus show that, at the low levels, GH gene expression in trout leucocytes is regulated by cortisol, which has been known as a regulatory factor of GH gene expression in pituitary cells, and suggest a physiological significance of paracrine GH produced in the fish immune system.

Details

Language :
English
ISSN :
0016-6480
Volume :
142
Issue :
1-2
Database :
MEDLINE
Journal :
General and comparative endocrinology
Publication Type :
Academic Journal
Accession number :
15862570
Full Text :
https://doi.org/10.1016/j.ygcen.2005.01.008