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https://hdl.handle.net/2440/77597
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Type: | Book chapter |
Title: | Roles of EGF family of growth factors in growth: overview of their roles in postnatal growth and development |
Author: | Xian, C. Shandala, T. |
Citation: | Handbook of Growth and Growth Monitoring in Health and Disease, 2012 / Preedy, V. (ed./s), pp.2857-2870 |
Publisher: | Springer |
Publisher Place: | United States |
Issue Date: | 2012 |
ISBN: | 9781441917942 |
Editor: | Preedy, V. |
Statement of Responsibility: | Cory J. Xian and Tetyana Shandala |
Abstract: | Ligands of the epidermal growth factor receptor (EGF-R), known to be important for supporting embryonic tissue development particularly in the gut and brain, have also been implicated in regulating postnatal somatic growth. While optimal levels of both milk-borne and endogenous EGF-R ligands are important for supporting postnatal somatic growth through regulating gastrointestinal growth and maturation, supra-physiological levels of EGF-R ligands can cause retarded and disproportionate growth and alter body composition as they increase growth of epithelial tissues but decrease masses of muscle, fat, and bone. EGF-R ligands can exert influence on growth indirectly via regulating levels of insulin-like growth factor (IGF-I) and its binding proteins (IGFBPs); EGFR ligands can also directly regulate bone growth and modeling, as they can enhance proliferation but suppress maturation of growth plate chondrocytes (for building a calcified cartilage scaffold for bone deposition) and osteoblasts (for depositing bone matrix), and promote formation and function of osteoclasts (for resorption of calcified cartilage or bone). In addition, EGF-R ligands, in particular amphiregulin, can themselves be regulated by parathyroid hormone (PTH), an important regulatory factor in bone modeling and remodeling. Finally, EGF-R ligands can regulate bone homeostasis by regulating pool of progenitor cells in the bone marrow through promoting their proliferation but suppressing differentiation of bone marrow mesenchymal stem cells. |
DOI: | 10.1007/978-1-4419-1795-9_170 |
Published version: | http://dx.doi.org/10.1007/978-1-4419-1795-9_170 |
Appears in Collections: | Aurora harvest 4 Molecular and Biomedical Science publications |
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