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differences in CYP expression occurs postpubertally) ( Shapiro et al . 1995 ). The only endogenous factor known to regulate the expression of adult hepatic CYP is growth hormone (GH) ( Legraverend et al . 1992 , Shapiro et al . 1995 ). At puberty, males
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Introduction The growth plate cartilage is responsible for achieving the longitudinal growth of long bones. Being a cartilage scaffold, the growth plate remains the weakest part of a long bone and hence prone to injury ( Mizuta et al . 1987
Department of spinal surgery, enji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
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Introduction The formation and growth of the axial and appendicular skeleton depend strictly on endochondral formation, which is initiated in the fetal stage and continues to adolescence ( Kronenberg 2003 ). The growth plate (GP) is located
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Introduction The epidermal growth factor receptor (EGFR), also called ERBB-1, belongs to a family of tyrosine kinase receptors (RTKs) that includes three additional proteins, ERBB-2, ERBB-3 and ERBB-4 ( Yarden & Sliwkowski 2001
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waste transport and modulating the maternal environment through the elaboration of an assortment of hormones, growth factors, and other regulatory molecules. Understanding mechanisms underlying the growth and development of the placenta is paramount to
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), is thought to regulate cellular proliferation and maturation ( Potter et al . 2006 ). Convincing evidence from the last decade shows that CNP is essential for postnatal skeletal growth ( Chusho et al . 2001 ). For example, contrived ( Olney 2006
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, leaving a cartilaginous growth plate between the primary and secondary ossification centres, as well as the prospective permanent articular cartilages at each end of the bone. The growth plate is responsible for longitudinal growth of bones. Skeletal
Department of Physiology, Department of Biological and Medical Sciences, Development and Neuroscience, University of Cambridge, Physiology Building, Downing Street, Cambridge CB2 3EG, UK
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& Forhead 2009 , 2013 ). Deficiency of thyroid hormones during intrauterine development impairs growth of the fetus and compromises its adaptation to extrauterine life ( Fowden et al . 1998 , Hillman et al . 2012 , Sferruzzi-Perri et al . 2013
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Introduction Transduction of cellular signals is critical for development of mature cells and tissues. The regulation of mitogenesis by growth factors such as epidermal growth factor (EGF), erbB ligands, platelet-derived growth
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By combining data from studies of multinodular non-toxic goitre (MNTG) with data from rat models of goitre induction and in vitro models, a map of the growth factors involved in goitrogenesis has been constructed. We have addressed the roles of the insulin-like growth factors, transforming growth factors, fibroblast growth factors, endothelins, etc. We hypothesise that an imbalance in the interactions between the various growth factor axes exists in MNTG which favours cell replication. Thyrotrophin, although not significantly elevated in MNTG, exerts critical effects through interactions with autocrine and paracrine factors and their receptors. Expansion of the thyroidal vascular bed through angiogenesis is closely co-ordinated with follicular cell expansion and folliculoneogenesis, and while the integrated paracrine actions of fibroblast growth factors, vascular endothelial growth factor and endothelin probably play central roles, additional, as yet elusive, factors are probably involved. The combination of in vitro and in vivo approaches, designed to address specific questions, will undoubtedly continue to prove invaluable in dissecting further the complex interactions that exist between these growth factors, their binding proteins and receptors in goitrogenesis.
