Regulation of Rapid Signal Transducer and Activator of Transcription-5 Phosphorylation in the Resting Cells of the Growth Plate and in the Liver by Growth Hormone and Feeding

Gevers, E. F., Hannah, M. J., Waters, M. J. and Robinson, I. C. A. F. (2009) Regulation of Rapid Signal Transducer and Activator of Transcription-5 Phosphorylation in the Resting Cells of the Growth Plate and in the Liver by Growth Hormone and Feeding. Endocrinology, 150 8: 3627-3636. doi:10.1210/en.2008-0985


Author Gevers, E. F.
Hannah, M. J.
Waters, M. J.
Robinson, I. C. A. F.
Title Regulation of Rapid Signal Transducer and Activator of Transcription-5 Phosphorylation in the Resting Cells of the Growth Plate and in the Liver by Growth Hormone and Feeding
Journal name Endocrinology   Check publisher's open access policy
ISSN 0013-7227
Publication date 2009-08-01
Year available 2009
Sub-type Article (original research)
DOI 10.1210/en.2008-0985
Open Access Status
Volume 150
Issue 8
Start page 3627
End page 3636
Total pages 10
Editor Jeffrey D Blaustein
Place of publication California, USA
Publisher The Endocrine Society
Language eng
Subject C1
9201 Clinical Health (Organs, Diseases and Abnormal Conditions)
920106 Endocrine Organs and Diseases (excl. Diabetes)
0604 Genetics
Abstract GH has physiological functions in many tissues, but the cellular targets for direct effects of GH remain ill defined in complex tissues such as the growth plate in which the contribution of direct vs. indirect actions of GH remains controversial. The Janus kinase (Jak)-signal transducer and activator of transcription (STAT)-5 pathway is activated by GH, so we developed a method to visualize nuclear Stat5b and phosphorylated Stat5 in single cells in response to a pulse of GH. Hep2 cells did not show a Stat5 phosphorylation (pY-Stat5) response to GH except in cells transfected to express GH receptors. ATDC5 cells express GH receptors and showed GH-induced pY-Stat5 responses, which varied with their state of chondrocyte differentiation. In vivo, Stat5b+ve nuclei were seen in the resting and prehypertrophic chondrocytes of the growth plate. After a single ip pulse of human GH or mouse GH, but not prolactin, pY-Stat5 responses were visible in cells in the resting zone and groove of Ranvier, 10–45 min later. Prehypertrophic chondrocytes showed no pY-Stat5 response to GH. GH target cells were also identified in other tissues, and a marked variability in spatiotemporal pY-Stat5 responses was evident. Endogenous hepatic pY-Stat5 was detected in mice with intact GH secretion but only during a GH pulse. Fasting and chronic exposure to GH attenuated the pY-Stat5 response to an acute GH injection. In conclusion, pY-Stat5 responses to GH vary in time and space, are sensitive to nutritional status, and may be inhibited by prior GH exposure. In the growth plate, our data provide direct in vivo support for an early role of GH to regulate the fate of immature chondrocytes.
Keyword LONGITUDINAL BONE-GROWTH
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: 2010 Higher Education Research Data Collection
Institute for Molecular Bioscience - Publications
 
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Created: Thu, 03 Sep 2009, 17:48:08 EST by Mr Andrew Martlew on behalf of Institute for Molecular Bioscience