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Submitted on November 3, 2003
Accepted on January 7, 2004
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Virginia, Charlottesville, Virginia, 22908; Edison Biotechnology Institute, Ohio University, Athens, Ohio 45701; Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701
* To whom correspondence should be addressed. E-mail: mot{at}virginia.edu.
Growth hormone (GH) has diverse biological actions that are mediated by binding to a specific, high affinity cell surface receptor (GHR). Expression of GHR is tissue-specific and a requirement for cellular responsiveness to GH. Insulin-like growth factor I (IGF-I) is produced in multiple tissues and regulated in part by GH through GHR. In this study we evaluated GHR and insulin-like growth factor I (IGF-I) mRNA expression in pituitary gland and compared the levels with those derived from liver of bovine GH transgenic (bGH), GH antagonist transgenic (GHA), lit/lit mice and their respective controls using real-time RT-PCR.
In liver, both GHR and IGF-I mRNA expressions were regulated in parallel with GH action in all 3 animal models and there was a strong correlation between GHR and IGF-I mRNA levels.
In pituitary gland, increased expression of IGF-I mRNA in the pituitary of bGH mice was observed whereas IGF-I expression in GHA or lit/lit mice was similar to that observed in control animals. There were no differences of GHR mRNA levels in pituitary gland of any groups we examined. There was also no correlation between GHR and IGF-I mRNA levels in any group in the pituitary gland.
In conclusion, we found that hepatic GHR and IGF-I mRNA levels were strongly correlated with each other in chronic GH excess or deficient state, and that regulation and correlation between local GHR and IGF-I mRNA levels induced by GH is different between liver and pituitary gland.
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