Id基因对BMP维持椎间盘细胞软骨特性的影响及作用机制研究

The degenerative disc disease is common in the elderly disease. the research of delaying disc degeneration is hot pot by the exogenous gene transfected. Bone morphogenefic proteins(BMP) is one of them that has the clinical application of treatment factor,but the specific mechanism is not clear.The research proves BMP may promote to expression of Id transcription factor in disc cells and interact with Id could promote the proliferation and differentiation of cartilage.Rabbit disc is intended to as the research object in this topic. By restructuring the adenoviruses system, intervention with intracellular expression of Id gene levels,cartilage cells characteristics matrix type Ⅱcollagen, proteoglycan,osteocalcin etc as detected objects, analyzes the effect of Id on BMP-2 maintaining disc cell phenotype cartilage effect,explicits regulating mechanism of Id gene on BMPs in intervertebral disc cells,And try to find a more ideal treatment disc degeneration of biology method and new ideas researching disc degeneration mechanism by BMPs signal transduction pathways.

退变性椎间盘疾病是老年人群中的常见疾病，通过外源性基因转染椎间盘细胞延缓退变是目前研究的热点，其中骨形态发生蛋白（BMP）是非常具有临床应用前景的治疗因子，但其具体作用机制尚不明确。研究证实，椎间盘细胞中BMP可以显著上调分化抑制因子Id的表达，Id分子作为重要的调节细胞活性状态的信号，可能与BMP信号系统相互作用以促进椎间盘细胞的增殖及软骨样基质的分泌。本课题拟以兔椎间盘细胞为研究对象，通过重组腺病毒体系，干预胞内Id的表达水平，以软骨细胞特性基质Ⅱ型胶原、蛋白多糖、成骨标志骨钙素等为检测对象，分析Id对BMP维持椎间盘细胞软骨表型作用的影响；并深入研究其与BMP信号通路下游分子Smads之间的关系，旨在分子水平明确Id对BMP维持椎间盘细胞软骨特性的调节机制，为今后从BMP信号转导途径入手，寻找一种治疗椎间盘退变更为理想的生物学方法提供理论依据和实验基础。