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Journal of Pediatric Endocrinology and Metabolism

Editor-in-Chief: Kiess, Wieland

Ed. by Bereket, Abdullah / Darendeliler, Feyza / Dattani, Mehul / Gustafsson, Jan / Luo, Fei Hong / Mericq, Veronica / Ogata, Tsutomu / Toppari, Jorma


IMPACT FACTOR 2017: 1.086

CiteScore 2017: 1.07

SCImago Journal Rank (SJR) 2017: 0.465
Source Normalized Impact per Paper (SNIP) 2017: 0.580

Online
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2191-0251
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Volume 25, Issue 9-10

Issues

Increased growth hormone receptor (GHR) degradation due to over-expression of cytokine inducible SH2 domain-containing protein (CIS) as a cause of GH transduction defect (GHTD)

Andrea Paola Rojas Gil
  • Corresponding author
  • Faculty of Human Movement and Quality of Life Sciences, Department of Nursing University of Peloponnese, Sparta, Greece
  • Research Laboratory of the Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University of Patras School of Medicine, Patras, Greece
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  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Eirini Kostopoulou
  • Research Laboratory of the Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University of Patras School of Medicine, Patras, Greece
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/ Ioulia Karageorgou
  • Research Laboratory of the Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University of Patras School of Medicine, Patras, Greece
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  • De Gruyter OnlineGoogle Scholar
/ Konstantinos Kamzelas
  • Research Laboratory of the Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University of Patras School of Medicine, Patras, Greece
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  • De Gruyter OnlineGoogle Scholar
/ Bessie Eugenia Spiliotis
  • Research Laboratory of the Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University of Patras School of Medicine, Patras, Greece
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Published Online: 2012-09-06 | DOI: https://doi.org/10.1515/jpem-2012-0174

Abstract

Objective: Children with growth hormone transduction defect (GHTD) have impaired growth and signal transducer and activator of transcription 3 (STAT3) activation. Here, we examine the etiology of GHTD.

Methods: Control (Cf) and GHTD (Pf) children’s fibroblasts were induced with hGH, MG132, lactacystin or silence RNA/CIS (siCIS). Western immunoblotting (WI) examined protein expression. Immunofluorescent microscopy (IF) examined cellular localization.

Results: (i) Pf showed retarded activation of pJAK2 and pSTAT-5 and increased ubiquitinated CIS (UbCIS) by WI. (ii) After MG132, Pf showed normal activation of pJAK2, pSTAT5 and pSTAT3. (iii) IF showed membrane (ML) and cytoplasmic localization (CL) of the GHR in Cf while the Pf showed only CL. In Pf, induction with lactacystin or siCIS changed the localization of the GHR to ML.

Conclusions: In GHTD, abnormal GH signalling may be caused by over-expression of CIS, which may increase degradation of GHR, thus reducing membrane GHR availability, delaying activation of pJAK2 and pSTAT5 and reducing activation of pSTAT3.

Keywords: cyclin-dependent kinase inhibitor p21/waf1/cip1; cytokine inducible SH2 domain-containing protein; growth hormone; growth hormone receptor; growth hormone transduction defect; proteasome inhibitor; signal transducer and activator of transcription; ubiquitin

About the article

Corresponding author: Andrea Paola Rojas Gil, Faculty of Human Movement and Quality of Life Sciences, Department of Nursing, University of Peloponnese, Orthias Artemidos and Plateon Sparta, Greece 23100, Phone: +27310-89720, Fax: +27310-89721


Received: 2012-06-05

Accepted: 2012-08-05

Published Online: 2012-09-06

Published in Print: 2012-10-01


Citation Information: Journal of Pediatric Endocrinology and Metabolism, Volume 25, Issue 9-10, Pages 897–908, ISSN (Online) 2191-0251, ISSN (Print) 0334-018X, DOI: https://doi.org/10.1515/jpem-2012-0174.

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