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作 者:俞文华[1] 白秀英 李平风[1] 李刚[1] 杜国光[1]
机构地区:[1]北京医科大学生物化学与分子生物学系,北京100083
出 处:《中国生物化学与分子生物学报》2000年第3期377-381,共5页Chinese Journal of Biochemistry and Molecular Biology
基 金:国家自然科学基金资助项目 !(3 9770 93 1 )
摘 要:间歇性小剂量地给予甲状旁腺素 (parathyroid hormone,PTH)可促进成骨 .胰岛素样生长因子 - I(insulin- like growth factor- I,IGF- I)由成骨细胞所产生并贮存于骨基质中 ,可促进成骨细胞的增殖分化 .为进一步了解向钙性激素和骨源性生长因子对骨生长的影响 ,利用成骨样细胞 ROS1 7/ 2 .8进行体外实验 ,观察了 PTH和 IGF- I这两种在骨生长和代谢中有重要作用的激素和因子相互作用的效果 ,并对其相互作用机制作出初步探讨 .结果显示 :联合使用 IGF- I及 PTH(间歇性给药 )时 ,(1 ) SRB(sodium rhodamine B,SRB)染色显示经 PTH(1 0 -9mol/ L,间歇给药 )和 IGF- I(1 0 -9mol/ L)联合处理的细胞 ,其数目明显增加 ,且明显高于单独处理组 ;(2 ) 3H- Td R参入增加 ,也明显高于单独处理组 ;(3)与增殖相关的原癌基因 (c- fos,c- jun,c- ki- ras)的表达增强 ,明显高于单独处理组 ;(4)骨钙素 (osteocalcin)基因 m RNA表达增强 ,明显高于单独处理组 ;(5) IGF- I(1 0 -8mol/L,1 0 -9mol/ L)可使 PTH受体基因 m RNA表达增强 .这些结果提示 PTH和 IGF- I在成骨样细胞ROS 1 7/ 2 .8增殖分化中具有协同作用 ,原癌基因的表达增强可能是其作用的一个环节 .此外 ,IGF- I可能通过增强 PTH受体表达 ,使细胞对It has been reported that parathyroid hormone (PTH) exerts bone forming effects in vivo when administered intermittently.Insulin like growth factor I(IGF I)is produced by osteoblasts and stored in the bone matrix.IGF I stimulates the proliferation and differentiation of osteoblast.To further understand the interaction between calciotropic hormones and those bone derived growth factors in osteoblasts,the interaction between PTH and IGF I in osteoblast like ROS 17/2.8 cells was observed,and the possible explanation of the mechanism was provided.Cells were exposed to IGF I(10 9 mol/L)for three days,meanwhile PTH(10 9 mol/L)was added for the first 6 hours of each day.The results showed that SRB(sodium rhodamine B)assay and 3H TdR incorporations were all significantly enhanced by the combined treatrment of PTH(intermittently)and IGF I.PTH combined with IGF I could also induce the gene expression of proto oncogene( c fos,c jun,c ki ras )and the marker protein of osteoblast osteocalcin gene.Furthermore,the gene expression of PTH receptor could be induced by IGF I.These data suggested that IGF I and PTH might synergistically stimulate proliferation and differentiation in osteoblast like ROS 17/2.8 cells.The enhanced gene expression of proto oncogene probably played a role in the mechanism.IGF I might regulate the response of the osteoblast like cell to PTH via enhancing the PTH receptor gene expression.
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