Expression of matrix metalloproteinase genes in the rat intramembranous bone during postnatal growth and upon mechanical stresses

被引:29
作者
Collins, JM [1 ]
Ramamoorthy, K [1 ]
Da Silveira, A [1 ]
Patston, P [1 ]
Mao, JJ [1 ]
机构
[1] Univ Illinois, Tissue Engn Lab, Chicago, IL 60612 USA
关键词
matrix metalloproteinase; bone; mechanical; stresses; cranial; sutures;
D O I
10.1016/j.jbiomech.2004.04.018
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
A cranial suture consists of neural-crest derived cells and matrices between mineralized skull bones. Little is known regarding the involvement of matrix metalloprotemases (MMPs) in the degradation of extracellular matrix of cranial sutures. In the postnatal rat model, the posterior frontal suture (PFS) undergoes complete ossification between P12-P22, whereas the sagittal suture (SS) remains patent. The present study utilized reverse transcriptase-polymerase chain reaction (RT-PCR) to explore the expression of MMP-1 and MMP-2 genes in the PFS and SS in P8 and P32 rats, and also to determine whether these MMP genes are modulated by exogenous mechanical forces. RNA was isolated from P8 and P32 normal PFS and SS each by pooling sutural specimens from 14 to 20 rats. RT-PCR analysis and semi-quantitative luminosity demonstrated the expression of MMP-1 and MMP-2 genes in the patent P8 PFS, P8 SS, and P32 SS, but no apparent MMP-2 expression in the physiologically ossified P32 PFS. Exogenous cyclic forces applied to the maxilla at 1000 mN and 4 Hz elicited corresponding cyclic bone strain waveforms with peak strain of 134.14 +/- 38.15 muepsilon (mean +/- S.D.) for the PFS, and 28.35 +/- 10.86 muepsilon for the SS in P32 rats. These cyclic forces delivered for 20 min/d over 2 consecutive days induced the expression of MMP-2 gene in the physiologically fused P32 PFS that was not expressed without mechanical stresses. Taken together, these data suggest potentially important roles of MMP genes in the postnatal development of cranial sutures, and their susceptibility to mechanical stresses. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:485 / 492
页数:8
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