Recombinant osteogenic protein-1 upregulates extracellular matrix metabolism by rabbit annulus fibrosus and nucleus pulposus cells cultured in alginate beads

被引:164
作者
Masuda, K
Takegami, K
An, H
Kumano, F
Chiba, K
Andersson, GBJ
Schmid, T
Thonar, E
机构
[1] Rush Presbyterian St Lukes Med Ctr, Rush Med Coll, Dept Orthoped Surg, Chicago, IL 60612 USA
[2] Rush Presbyterian St Lukes Med Ctr, Rush Med Coll, Dept Biochem, Chicago, IL 60612 USA
[3] Rush Presbyterian St Lukes Med Ctr, Rush Med Coll, Dept Internal Med, Chicago, IL 60612 USA
关键词
intervertebral disc; osteogenic protein-1; bone morphogenetic protein-7; extracellular matrix; proteoglycan; collagen;
D O I
10.1016/S0736-0266(03)00037-8
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
This study was performed to determine if recombinant human osteogenic protein-1 (rhOP-1) is effective in promoting matrix synthesis and matrix formation by rabbit nucleus pulposus (NP) and annulus fibrosus (AF) cells cultured in alginate beads. The effects of culturing the cells in the presence of various concentrations of rhOP-1 were assessed by measuring changes in cell proliferation, proteoglycan (PG) and collagen synthesis and mRNA expression, and in the matrix contents of PG and collagen, as indicators of matrix accumulation. At high concentrations, rhOP-1 had a moderate mitogenic effect on both NP and AF cells. It also stimulated the synthesis of PG and collagen in a dose-dependent manner: this was associated with a corresponding increase in the expression of mRNA for aggrecan core protein and collagen type II. The stimulatory effect of rhOP-1 on PG synthesis was more pronounced than that on collagen synthesis. Continuous treatment with rhOP-1 led to an increase in the total DNA, PG and collagen contents in both NP and AF cultures. The results presented here provide evidence of the ability of rhOP-1 to stimulate the metabolism of both rabbit AF and NP cells cultured in alginate beads. (C) 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:922 / 930
页数:9
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