Shared pathways of osteoblast mitogenesis induced by amylin, adrenomedullin, and IGF-1

Amylin and adrenomedullin, members of the calcitonin peptide family, are anabolic to bone. Here, we report overlapping molecular mechanisms by which amylin, adrenomedullin, and IGF-1 induce osteoblast proliferation. Co-treatment of osteoblastic cells with amylin or adrenomedullin and IGF-1 failed to...

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Bibliographic Details
Published in:	Biochemical and biophysical research communications Vol. 318; no. 1; pp. 240 - 246
Main Authors:	Cornish, Jillian, Grey, Andrew, Callon, Karen E, Naot, Dorit, Hill, Bernadine L, Lin, Cindy Q.X, Balchin, Leanne M, Reid, Ian R
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 21-05-2004
Subjects:	Adrenomedullin Amyloid - metabolism Amyloid - pharmacology Animals Calcitonin-like Cell Division - drug effects Cells, Cultured Enzyme Activation - drug effects Fibroblasts - metabolism GTP-Binding Protein alpha Subunits, Gi-Go - metabolism Humans IGF-1 receptor In vitro Insulin-Like Growth Factor I - antagonists & inhibitors Insulin-Like Growth Factor I - pharmacology Islet Amyloid Polypeptide MAP-kinase Mice Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases - metabolism Mitogens - pharmacology Osteoblast Osteoblasts - cytology Osteoblasts - drug effects Peptides - metabolism Peptides - pharmacology Rats Receptor, IGF Type 1 - metabolism Receptors, Islet Amyloid Polypeptide Receptors, Peptide - antagonists & inhibitors Signal Transduction Transforming Growth Factor beta - pharmacology Osteoblast Calcitonin-like MAP-kinase In vitro IGF-1 receptor
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Summary:	Amylin and adrenomedullin, members of the calcitonin peptide family, are anabolic to bone. Here, we report overlapping molecular mechanisms by which amylin, adrenomedullin, and IGF-1 induce osteoblast proliferation. Co-treatment of osteoblastic cells with amylin or adrenomedullin and IGF-1 failed to induce an additive mitogenic effect. In osteoblastic cells, neutralization of the IGF-1 receptor blocked the proliferative effects of amylin and adrenomedullin, while neutralization of IGF-1 did not. Neither amylin- nor adrenomedullin-induced mitogenic signaling or cell proliferation in IGF-1 receptor-null fibroblasts. In addition, amylin and adrenomedullin receptor blockers inhibited the proliferative effects of IGF-1 in osteoblastic cells. These findings demonstrate overlap in the molecular mechanisms by which amylin, adrenomedullin, and IGF-1 induce mitogenesis in osteoblasts, and an important role for the IGF-1 receptor in the mitogenic actions of amylin and adrenomedullin. Our findings are potentially important in refining these peptides for the therapy of osteoporosis.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0006-291X 1090-2104
DOI:	10.1016/j.bbrc.2004.04.020