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

被引：40

作者：

Cornish, J ^{[1
]}

Grey, A ^{[1
]}

Callon, KE ^{[1
]}

Naot, D ^{[1
]}

Hill, BL ^{[1
]}

Lin, CQX ^{[1
]}

Balchin, LM ^{[1
]}

Reid, IR ^{[1
]}

机构：

[1] Univ Auckland, Dept Med, Auckland, New Zealand

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 318卷 / 01期

关键词：

osteoblast; calcitonin-like; in vitro; MAP-kinase; IGF-1; receptor;

D O I：

10.1016/j.bbrc.2004.04.020

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 ostcoblastic 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. (C) 2004 Elsevier Inc. All rights reserved.

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页码：240 / 246

页数：7

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