摘要
软骨细胞的老化是一个极其复杂的过程,其特征包括:细胞不可逆的生长停滞于G1期;老化相关β-半乳糖苷酶的表达;端粒长度缩短;软骨细胞分化特征的改变。目前认为其机制为基因表达的程序性或减进性改变,包括肿瘤抑制基因p53和pRb等在细胞生长停滞中的作用;端粒结合蛋白和端粒酶对端粒长度的调节;细胞骨架蛋白的重组使软骨细胞形态的变化;基质降解酶类表达增加以及各种细胞因子的变化对软骨细胞代谢的影响。
Senescence of chondrocytes is clearly a complex process. The phenotypes of senescent chondrocytes includes irreversible growth arrest: senescence-associated-gal (SA-gal) expression, telomere shortening, and altered differentiation. Senescence is very likely due to programmed changes in gene expression, such as the cells arrest growth due to altered tumor suppressors p53 and pRb, telomerase and telomere associated proteins regulate the length of telomere, reorganization of the actin cytoskeleton leads to the change of cell morphology, over expression of matrix degradation proteases, and the change of cytokines interference metabolism of chondrocytes.
出处
《上海第二医科大学学报》
CSCD
2004年第4期322-324,F003,共4页
Acta Universitatis Medicinalis Secondae Shanghai
基金
国家重点基础研究发展规划资助项目("973"项目)(G1999054304)
上海市"重中之重"重点学科基金资助.