Up-regulation of insulinlike growth factor I binding sites in experimental colitis in rats.
Up-regulation of insulinlike growth factor I binding sites in experimental colitis in rats.
复制标题
大鼠实验性结肠炎中胰岛素样生长因子 I 结合位点的上调。
DOI：
10.1016/0016-5085(95)90435-2
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发表时间：
1995
期刊：
影响因子：
29.4
通讯作者：
McRoberts,JA
中科院分区：
文献类型：
--
作者：
Zeeh,JM;Hoffmann,P;Sottili,M;Eysselein,VE;McRoberts,JA
背景/目的胃肠道是胰岛素样生长因子（IGF）I的主要靶点。IGF-I结合两种不同的受体和结合蛋白（IGFBPs），作为载体和介质。本研究探讨了IGF-I结合位点在大鼠colis.Methodscolitis的调节，结肠滴注的2，4，6-三硝基苯磺酸在乙醇中诱导。通过与125 I-IGF-I孵育来定位结肠切片中的IGF-I结合位点。通过与未标记IGF-I、IGF-II和胰岛素竞争，估计与IGF-I受体结合的贡献。结果损伤后12小时至1周，炎症结肠固有肌层中的IGF-I结合位点增加了两倍以上。通过北方杂交筛选结肠RNA中的IGFBPs。胰岛素不能取代这种高水平的结合，即使它可以取代IGF-I从粘膜和粘膜肌层。北方杂交显示IGFBP-4和IGFBP-5信使RNA从发炎colon.ConclusionsExperimental结肠炎大鼠引起IGF-I结合固有肌层，这代表IGFBP-4和IGFBP-5的水平增加2-3倍增加。这些数据表明IGFBPs在炎症和组织修复过程中调节IGF作用的重要作用。
Background/AimsThe gastrointestinal tract is a major target of insulinlike growth factor (IGF) I. IGF-I binds to two different receptors and to binding proteins (IGFBPs), which act as carriers and mediators. This study investigated the regulation of IGF-I binding sites in rat colitis.MethodsColitis was induced by colonic instillation of 2,4,6-trinitrobenzenesulfonic acid in ethanol. IGF-I binding sites in colon sections were localized by incubation with125I-IGF-I. The contribution of binding to the IGF-I receptor was estimated by competition with unlabeled IGF-I, IGF-II, and insulin. Colonic RNA was screened for IGFBPs by Northern hybridization.ResultsIGF-I binding sites were increased more than two-fold in the muscularis propria of inflamed colon as soon as 12 hours and up to 1 week after injury. Insulin could not displace this elevated level of binding, even though it could displace IGF-I from the mucosa and muscularis mucosa. Northern hybridization showed a 2–3-fold increase in IGFBP-4 and IGFBP-5 messenger RNA from inflamed colon.ConclusionsExperimental colitis in rats causes an increase in IGF-I binding to the muscularis propria, which represents increased levels of IGFBP-4 and IGFBP-5. These data suggest an important role for IGFBPs in modulating IGF effects during inflammation and tissue repair.