Insulin-like growth factor I and insulin-like growth factor binding protein 5 in Crohn's disease.
Insulin-like growth factor I and insulin-like growth factor binding protein 5 in Crohn's disease.
复制标题
克罗恩病中的胰岛素样生长因子 I 和胰岛素样生长因子结合蛋白 5。
DOI：
10.1152/ajpgi.2001.280.5.g1022
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Pucilowska,JB
中科院分区：
文献类型：
--
作者：
Zimmermann,EM;Li,L;Hou,YT;Mohapatra,NK;Pucilowska,JB
胰岛素样生长因子(IGF)- 1及其结合蛋白IGF结合蛋白5 （IGFBP-5）在实验性克罗恩病炎症和纤维化肠中高表达。igf - 1诱导平滑肌细胞和成纤维细胞/肌成纤维细胞增殖并增加胶原合成。我们研究了克罗恩病组织中的igf - 1和IGFBP-5。组织收集于因克罗恩病而接受肠切除术的患者。IGF-I和IGFBP-5 mrna分别通过RNase保护实验和Northern blot分析进行定量。原位杂交定位mRNA表达，Western免疫印迹法定量蛋白表达。与正常肠相比，炎症/纤维化肠中IGF-I和IGFBP-5 mrna升高。IGF-I mRNA在粘膜下层和外肌层固有层和成纤维细胞样细胞中多种细胞类型中表达。IGFBP-5 mRNA在粘膜肌层和外肌层的平滑肌以及整个肠壁的成纤维细胞样细胞中高表达。组织IGFBP-5蛋白与I型胶原相关（r= 0.82）。这些发现与igf - 1作用于平滑肌和成纤维细胞/肌成纤维细胞以增加胶原合成和细胞增殖的机制一致；其作用可能由局部表达的IGFBP-5调节。
Insulin-like growth factor (IGF)-I and its binding protein IGF binding protein 5 (IGFBP-5) were highly expressed in inflamed and fibrotic intestine in experimental Crohn's disease. IGF-I induced proliferation and increased collagen synthesis by smooth muscle cells and fibroblasts/myofibroblasts in vitro. Here we studied IGF-I and IGFBP-5 in Crohn's disease tissue. Tissue was collected from patients undergoing intestinal resection for Crohn's disease. IGF-I and IGFBP-5 mRNAs were quantitated by RNase protection assay and Northern blot analysis, respectively. In situ hybridization was performed to localize mRNA expression, and Western immunoblot was performed to quantitate protein expression. IGF-I and IGFBP-5 mRNAs were increased in inflamed/fibrotic intestine compared with normal-appearing intestine. IGF-I mRNA was expressed in multiple cell types in the lamina propria and fibroblast-like cells of the submucosa and muscularis externa. IGFBP-5 mRNA was highly expressed in smooth muscle of the muscularis mucosae and muscularis externa as well as fibroblast-like cells throughout the bowel wall. Tissue IGFBP-5 protein correlated with collagen type I (r= 0.82). These findings are consistent with a mechanism whereby IGF-I acts on smooth muscle and fibroblasts/myofibroblasts to increase collagen synthesis and cellular proliferation; its effects may be modulated by locally expressed IGFBP-5.