Regulation mechanism of nsulin-like growth factor-binding proteins producion in osteoarthritis.

软骨组织的破坏导致骨关节炎的功能残疾。软骨组织的修复被认为在这种疾病中受到了干扰。胰岛素样生长因子（IGF）是软骨细胞的合成代谢因子，受结合蛋白（IGPBPs）调节。我们假设igf - 1对软骨细胞的作用在骨关节炎中受到干扰。因此，我们试图研究人软骨细胞产生的igfbp，它可能调节IGE的作用。采用Western-ligand blotting （WLB）和免疫沉淀法，发现永生化的人软骨细胞分泌IGFBP-2、-3、-4和-5。用igf - 1处理细胞导致IGFBP-5的剂量依赖性增加。通过亲和交联法检测与细胞膜相关的igfbp，发现IGFBP-3和-5以及1型LGF和2型[GE]受体。为了明确骨关节炎中igfbp的变化，在培养基中加入白细胞介素-1b。不幸的是，无论是否有白细胞介素-1，他们之间都没有差异。我们应该利用手术标本获得的人软骨组织进一步研究IGEBP在骨关节炎中产生的调控机制。

Thc destruction of cartilage tissue causes functional disability in osteoarthritis. The repair of cartilage tissue are supposed to be disturbed in this disease. Insulin-like growth factor (IGF) is an anabolic factor for chondrocytes and is regulated by binding proteins (IGPBPs). We assumed that the effect of IGF-I on chondrocytes are disturbed in osteoarthritis. So we tried to study the IGFBPs produced by human chondrocytes, which may regulate IGE action. Employing Western-ligand blotting (WLB) and immunoprecipitation, immortalized humah chondrocytes were found to secrete IGFBP-2, -3, -4 and -5. Treatment of cells with IGF-I resulted in a dose-dependent increase of IGFBP-5. The IGFBPs associated with cell membrane were examined by affinity cross-linking method, showing the IGFBP-3 and -5 as well as type 1 LGF and type 2 [GE receptor. To clarify the changes of IGFBPs in osteoarthritis, interleukin-1b is added to the culture medium. Unfortunately, there was no difference between them, with /without interleukin-1. We should further study the regulation mechanism of IGEBP production in osteoarthritis by using human cartilage tissue obtained by operated sample.