Radisky D C, Kaplan J
Department of Pathology, University of Utah Health Sciences Center, Salt Lake City, UT 84132, USA.
Biochem J. 1998 Nov 15;336 ( Pt 1)(Pt 1):201-5. doi: 10.1042/bj3360201.
Examination of the mechanism of intracellular iron recovery from lysosomally-degraded ferritin in vivo has been complicated by the continuous flux of cellular iron through ferritin molecules. Here we incubated human fibroblasts with cationic ferritin, a derivative of horse spleen ferritin, as a technique for delivering immunologically distinct ferritin molecules directly to lysosomes. Using this method, we found increased endogenous ferritin levels after the cellular degradation of cationic ferritin, demonstrating that cells can utilize lysosomal ferritin to produce increased cytosolic ferritin levels. Further, using an in vitro assay, we showed that isolated lysosomes degrade endogenous ferritin in a time- and temperature-dependent manner. These results are consistent with a model in which cytosolic ferritin is taken into the lysosomes and degraded. The solubilized iron from the ferric core could then be transported across the lysosomal membrane back into the cytosol.
体内细胞从经溶酶体降解的铁蛋白中回收细胞内铁的机制研究因细胞内铁通过铁蛋白分子的持续流动而变得复杂。在此,我们将人成纤维细胞与阳离子铁蛋白(马脾铁蛋白的衍生物)一起孵育,作为将免疫上不同的铁蛋白分子直接递送至溶酶体的技术。使用该方法,我们发现在阳离子铁蛋白细胞降解后内源性铁蛋白水平升高,表明细胞可以利用溶酶体铁蛋白来提高胞质铁蛋白水平。此外,通过体外试验,我们表明分离的溶酶体以时间和温度依赖性方式降解内源性铁蛋白。这些结果与一种模型一致,即胞质铁蛋白被摄取到溶酶体中并被降解。来自铁核的溶解铁然后可以穿过溶酶体膜回到胞质溶胶中。