Mechanical compression alters gene expression and extracellular matrix synthesis by chondrocytes cultured in collagen I gels

被引:124
作者
Hunter, CJ
Imler, SM
Malaviya, P
Nerem, RM
Levenston, ME
机构
[1] Georgia Inst Technol, Wallace H Coulter Dept Biomed Engn, Atlanta, GA 30332 USA
[2] Georgia Inst Technol, George W Woodruff Sch Mech Engn, Atlanta, GA 30332 USA
[3] Georgia Inst Technol, Parker H Petit Inst Bioengn & Biosci, Atlanta, GA 30332 USA
关键词
tissue engineering; collagen; chondrocyte; PCR; mechanical stimulation;
D O I
10.1016/S0142-9612(01)00245-9
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Articular cartilage responds to its mechanical environment through altered cell metabolism and matrix synthesis. In this study, isolated articular chondrocytes were cultured in collagen type I gels and exposed to uniaxial static compression of 0%, 25%, or 50% of original thickness for 0.5, 4, and 24 h, and to oscillatory (25 +/-4%, 1 Hz) compression for 24 h. The cellular response was assessed through competitive and real-time RT-PCR to quantify expression of genes for collagen type I, collagen type II, and aggrecan core protein, and through radiolabelled proline and sulfate incorporation to quantify protein and proteoglycan synthesis rates. Static compression for 24h inhibited expression of collagen I and II mRNAs and inhibited (3) H-proline and S-35-sulfate incorporation. The mRNA expression exhibited transient fluctuations at intermediate time points. Oscillatory compression had no effect upon mRNA expression, and 24 h after release from static compression, there was no difference in collagen II or aggrecan mRNA, while there was an inhibition of collagen I. We conclude that the chondrocytes maintained some aspects of their ability to sense and respond to static compression. despite a biochemical and mechanical environment which is different from that in tissue, This suggests that mechanical stimuli may be useful in modulating chondrocyte metabolism in tissue engineering systems using fibrillar protein scaffolds. (C) 2001 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:1249 / 1259
页数:11
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