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Changes with Age and the Effect of Recombinant Human BMP-2 on Proteoglycan and Collagen Gene Expression in Rabbit Anulus Fibrosus Cells

Changes with Age and the Effect of Recombinant Human BMP-2 on Proteoglycan and Collagen Gene Expression in Rabbit Anulus Fibrosus Cells

作     者:Hideki MURAKAMI Kai-Jow TSAI William C.HUTTON 

作者机构:Atlanta Veteran's Administration Medical CenterDecatur 30033USA Department of Orthopaedics and Spine CenterEmory University School of MedicineAtlanta 30329USA 

出 版 物:《Acta Biochimica et Biophysica Sinica》 (生物化学与生物物理学报(英文版))

年 卷 期:2006年第38卷第11期

页      面:773-779页

核心收录:

学科分类:0710[理学-生物学] 0831[工学-生物医学工程(可授工学、理学、医学学位)] 1001[医学-基础医学(可授医学、理学学位)] 0703[理学-化学] 10[医学] 

主  题:ageing anulus fibrosus cells bone morphogenetic protein-2 

摘      要:In order to compare the difference between young and old intervertebral disc cells and theirresponsiveness to recombinant human bone morphogenetic protein-2 (rhBMP-2),disc cells were isolatedfrom the anulus fibrosus (AF) and transition zones of lumbar discs from eight old and eight young NewZealand white *** with the ceils from the young rabbits,cells from old rabbits respond less torhBMP-2 treatment with respect to sulfated-glycosaminoglycan (sGAG) synthesis and aggrecan *** in collagen Ⅰ and collagen Ⅱ gene expressions,there are no significant differences betweenthe old and the *** comparing sGAG content,aggrecan,and collagen Ⅱ gene expression of the oldAF cells after rhBMP-2 treatment with that of the young AF cells without rhBMP-2 treatment,the old AFcells with rhBMP-2 treatment have a greater capacity to synthesize sGAG bound in the cells and to releasesGAG in the media,as well as to express aggrecan and collagen Ⅱ *** can be concluded that old AF cellsafter rhBMP-2 treatment have a greater capacity to synthesize sGAG and express aggrecan and collagen Ⅱ ascompared to young AF cells without rhBMP-2 *** rhBMP-2 can reverse the decline in theanabolic capacity of the disc cells with *** it seems that rhBMP-2 has potential for use as an agent toretard a key component of disc degeneration and loss of disc matrix.

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