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

软骨组织的破坏会导致骨性关节炎的功能障碍。在这种疾病中，软骨组织的修复被认为是被干扰的。胰岛素样生长因子(IGF)是一种软骨细胞合成代谢因子，受结合蛋白(IGPBPs)调节。我们推测IGF-I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IGFBPs，它可能调节IGE的作用。采用Western-Ligand blotting和免疫沉淀方法，发现永生化人软骨细胞分泌IGFBP-2、-3、-4和-5。细胞经IGF-I处理后，IGFBP-5的表达呈剂量依赖性增加。亲和交联法检测到与细胞膜相关的IGFBP-3和IGFBP-5，以及1型LGF和2型[GE受体]。为了阐明IGFBPs在骨关节炎中的变化，在培养液中加入IL-1b。不幸的是，在有或没有白细胞介素1的情况下，它们之间没有区别。利用手术标本获得的人软骨组织，进一步研究IGEBP在骨性关节炎中产生的调节机制。

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.