Vibratory loading decreases extracellular matrix and matrix metalloproteinase gene expression in rabbit annulus cells.
BACKGROUND
Whole body vibration is an important factor contributing to low back and radicular pain. Vibratory loading as a mechanical stimulus is transferred to connective tissues as energy from ground reaction forces, as well as a direct input from the use of motorized tools and vehicles. Extracellular matrix degradation parallels increased age and mechanical stimuli resulting in disc degeneration and eventual spinal deformity.


OBJECTIVE
The objective of this study was to investigate the relationship between vibratory loading and extracellular matrix expression in cultured rabbit annulus cells.


METHODS
An in vitro rabbit model using cultured annulus fibrosis cells isolated from normal intervertebral disc was used to study matrix and metalloproteinase expression in response to vibration.


METHODS
Annulus fibrosis cells were isolated by collagenase digestion from New Zealand White rabbits. Vibratory stimulation was applied to annulus cells in vitro, using an oscillating platform to deliver 0.1 x gravity load at 6 Hz for 2, 4, 6 or 8 hours. Gene expression was assessed by reverse transcriptase polymerase chain reaction.


RESULTS
Aggrecan, collagen Type III and matrix metalloproteinase-3 gene expression was suppressed by vibratory loading in rabbit annulus cells. Suppression of the aggrecan gene might lead to a decrease in proteoglycan synthesis.


CONCLUSIONS
These data suggest that vibratory load may play an important role in extracellular matrix metabolism of intervertebral disc cells, especially in the gene expression pathway of proteoglycans. It has been proposed that vibratory loading increases production of matrix-degrading, proteolytic enzymes. We have demonstrated that gene expression for key matrix messages and matrix metalloproteinase is decreased by vibration. In conclusion, we believe that study of the roles between extracellular matrix gene suppression and mechanical stress may clarify the pathomechanism of disc degeneration, such as disc herniation or degeneration.
Department of Orthopaedics, 253 Burnett Womack Building, CB 7055, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7055, USA.
Satoru
S
Yamazaki
Albert J
AJ
Banes
Paul S
PS
Weinhold
Mari
M
Tsuzaki
Mamoru
M
Kawakami
Joe T
JT
Minchew
D053674:Aggrecans; D000818:Animals; D001483:Base Sequence; D002478:Cells, Cultured; D016326:Extracellular Matrix Proteins; D005260:Female; D005786:Gene Expression Regulation; D007403:Intervertebral Disc / Q000166:cytology; D037181:Lectins, C-Type; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000235:genetics* / Q000378:metabolism; D020778:Matrix Metalloproteinase 2 / Q000235:genetics* / Q000378:metabolism; D023421:Models, Animal; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D011509:Proteoglycans / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis; D011817:Rabbits; D012680:Sensitivity and Specificity; D013314:Stress, Mechanical; D014732:Vibration / Q000009:adverse effects*
D053674:Aggrecans; D016326:Extracellular Matrix Proteins; D037181:Lectins, C-Type; D011509:Proteoglycans; D012333:RNA, Messenger; D020778:Matrix Metalloproteinase 2; D020781:Matrix Metalloproteinase 1