Yu G S, Hu J, Nakagawa H
R & D Center, BML, Kawagoe City, Saitama, Japan.
Neurosci Lett. 1998 Oct 2;254(3):125-8. doi: 10.1016/s0304-3940(98)00685-5.
Midkine (MK) is a neurotrophic and angiogenic growth factor whose expression occurs mainly in fetus. It was reported that MK was present in senile plaques of Alzheimer's disease (AD). To investigate the role of MK during amyloid plaques formation in AD, we examined the in vitro effect of MK on Abeta aggregation and Abeta-induced cytotoxicity. We found that incubation of MK with Abeta resulted in the formation of MK/Abeta complexes. The C-terminus of MK (60-121) played a similar role as the full length MK in complex formation. This interaction of MK and Abeta demonstrated significant inhibition on Abeta self-aggregation. MK also inhibited the cytotoxicity of Abeta on PC12h cells. These findings suggest that MK protects the cells from Abeta-induced cytotoxicity through its complex formation with Abeta. MK is probably expressed to prevent cell death in AD.
中期因子（MK）是一种神经营养和血管生成生长因子，其表达主要发生在胎儿期。据报道，MK存在于阿尔茨海默病（AD）的老年斑中。为了研究MK在AD淀粉样斑块形成过程中的作用，我们检测了MK对β淀粉样蛋白（Aβ）聚集和Aβ诱导的细胞毒性的体外作用。我们发现MK与Aβ孵育会导致MK/Aβ复合物的形成。MK的C末端（60 - 121）在复合物形成中与全长MK发挥相似作用。MK与Aβ的这种相互作用对Aβ自身聚集表现出显著抑制作用。MK还抑制了Aβ对PC12h细胞的细胞毒性。这些发现表明，MK通过与Aβ形成复合物来保护细胞免受Aβ诱导的细胞毒性。MK可能是为了预防AD中的细胞死亡而表达的。
