Shared pathways of osteoblast mitogenesis induced by amylin, adrenomedullin, and IGF-1 |
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Authors: | Cornish Jillian Grey Andrew Callon Karen E Naot Dorit Hill Bernadine L Lin Cindy Q X Balchin Leanne M Reid Ian R |
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Institution: | Department of Medicine, University of Auckland, Private Bag 92019, Auckland, New Zealand. j.cornish@auckland.ac.nz |
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Abstract: | 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. |
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Keywords: | Osteoblast Calcitonin-like In vitro MAP-kinase IGF-1 receptor |
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