亨廷顿舞蹈症患者纹状体中βII蛋白激酶C的缺失。

The loss of beta II-protein kinase C in the striatum from patients with Huntington's disease.

作者信息

Hashimoto T, Kitamura N, Saito N, Komure O, Nishino N, Tanaka C

机构信息

Department of Pharmacology, Kobe University School of Medicine, Japan.

出版信息

Brain Res. 1992 Jul 10;585(1-2):303-6. doi: 10.1016/0006-8993(92)91224-3.

DOI:10.1016/0006-8993(92)91224-3

PMID:1387337

Abstract

We have examined the levels of protein kinase C (PKC) in autopsied brains of patients with Huntington's disease (HD), using [3H]4-beta-phorbol-12,13-dibutyrate ([3H] PDBu) and antisera against the PKC subspecies. In the caudate nucleus and putamen from patients with HD, the specific binding for [3H]PDBu was significantly decreased by 74 and 68%, respectively, as compared to findings in controls. The beta II-PKC immunoreactivities were significantly reduced by 65%, whereas the alpha-PKC immunoreactivities increased by 146%, in the putamen. There were no differences in the beta I- or gamma-PKC immunoreactivities in the putamen between HD and controls. These results suggest the differential localization of four PKC subspecies in human striatum and the involvement of four subspecies in different aspects of HD pathophysiology.

摘要

我们使用[3H]4-β-佛波醇-12,13-二丁酸酯（[3H]PDBu）和针对蛋白激酶C（PKC）亚型的抗血清，检测了亨廷顿舞蹈病（HD）患者尸检大脑中的PKC水平。与对照组相比，HD患者尾状核和壳核中[3H]PDBu的特异性结合分别显著降低了74%和68%。壳核中βII-PKC免疫反应性显著降低了65%，而α-PKC免疫反应性增加了146%。HD患者与对照组壳核中βI-或γ-PKC免疫反应性没有差异。这些结果表明，四种PKC亚型在人类纹状体中定位不同，且四种亚型参与了HD病理生理学的不同方面。