Sparr Emma, Engel Maarten F M, Sakharov Dmitri V, Sprong Mariette, Jacobs Jet, de Kruijff Ben, Höppener Jo W M, Killian J Antoinette
Department Biochemistry of Membranes, Centre of Biomembranes and Lipid Enzymology, Institute of Biomembranes, Utrecht University, Padualaan 8, NL-3584 CH Utrecht, The Netherlands.
FEBS Lett. 2004 Nov 5;577(1-2):117-20. doi: 10.1016/j.febslet.2004.09.075.
Fibril formation of islet amyloid polypeptide (IAPP) is associated with cell death of the insulin-producing pancreatic beta-cells in patients with Type 2 Diabetes Mellitus. A likely cause for the cytotoxicity of human IAPP is that it destroys the barrier properties of the cell membrane. Here, we show by fluorescence confocal microscopy on lipid vesicles that the process of hIAPP amyloid formation is accompanied by a loss of barrier function, whereby lipids are extracted from the membrane and taken up in the forming amyloid deposits. No membrane interaction was observed when preformed fibrils were used. It is proposed that lipid uptake from the cell membrane is responsible for amyloid-induced membrane damage and that this represents a general mechanism underlying the cytotoxicity of amyloid forming proteins.
胰岛淀粉样多肽(IAPP)的纤维形成与2型糖尿病患者中产生胰岛素的胰腺β细胞的细胞死亡有关。人IAPP细胞毒性的一个可能原因是它破坏了细胞膜的屏障特性。在这里,我们通过对脂质囊泡的荧光共聚焦显微镜观察表明,hIAPP淀粉样蛋白形成过程伴随着屏障功能的丧失,由此脂质从膜中被提取出来并被吸收到正在形成的淀粉样沉积物中。当使用预先形成的纤维时,未观察到膜相互作用。有人提出,从细胞膜摄取脂质是淀粉样蛋白诱导的膜损伤的原因,并且这代表了淀粉样蛋白形成蛋白细胞毒性的一般机制。