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泛素羧基末端水解酶PGP 9.5在脊髓压迫性损伤后轴突中的表达。大鼠的免疫组织化学研究。

Expression of the ubiquitin carboxyl-terminal hydrolase PGP 9.5 in axons following spinal cord compression trauma. An immunohistochemical study in the rat.

作者信息

Li G L, Farooque M, Holtz A, Olsson Y

机构信息

Laboratory of Neuropathology, University Hospital, Uppsala, Sweden.

出版信息

APMIS. 1997 May;105(5):384-90. doi: 10.1111/j.1699-0463.1997.tb00585.x.

Abstract

Protein gene product 9.5 (PGP 9.5) is a neuron-specific protein which acts as a ubiquitin carboxyl-terminal hydrolase. It facilitates the conversion of polyubiquitin to monoubiquitin, which can be reused for another catalytic cycle. Monoubiquitin plays an important role in degrading abnormal and denatured proteins. Previously, we have reported that ubiquitin-like immunoreactivity is expressed in axonal swellings following compression trauma to the rat thoracic cord. It was characterized by fast occurrence, progressive increase and gradual disappearance over a period of 9 days. The expression of PGP 9.5 has now been studied in the same material. Control rats showed a weak PGP 9.5 immunoreactivity in the nerve cell bodies of the cord. Except for the corticospinal tracts, the axons of other longitudinal tracts were weakly stained. Accumulation of PGP 9.5 immunoreactivity occurred in expanded axons at the site of compression already 4 h after trauma. They became more frequent in number 1 and 4 days after injury and remained so over the entire observation period of 9 days. The labelled axons were randomly distributed in the longitudinal tracts, but were never found in the corticospinal tracts. The extent of immunoreactivity was related to the degree of impact on the cord. Compression injury thus induces accumulation of both ubiquitin and PGP 9.5 immunoreactivity in axonal expansions. The injured axons may have a mechanism for degradation of proteins by the ubiquitin-mediated proteolytic pathway and another mechanism for effective ubiquitin regenerative cycling by the action of PGP 9.5.

摘要

蛋白质基因产物9.5(PGP 9.5)是一种神经元特异性蛋白,具有泛素羧基末端水解酶的功能。它有助于将多聚泛素转化为单泛素,单泛素可再次用于另一个催化循环。单泛素在降解异常和变性蛋白质方面发挥着重要作用。此前,我们报道过,在大鼠胸段脊髓受到压迫性创伤后,轴突肿胀处会出现泛素样免疫反应。其特点是快速出现、逐渐增加并在9天内逐渐消失。现在已对同一材料中PGP 9.5的表达进行了研究。对照大鼠脊髓神经细胞体中PGP 9.5免疫反应较弱。除皮质脊髓束外,其他纵向束的轴突染色较弱。创伤后4小时,PGP 9.5免疫反应性就在压迫部位的扩张轴突中积聚。损伤后1天和4天,它们的数量变得更多,并在整个9天的观察期内一直如此。标记的轴突随机分布在纵向束中,但在皮质脊髓束中从未发现。免疫反应的程度与对脊髓的影响程度相关。因此,压迫性损伤会诱导轴突扩张中泛素和PGP 9.5免疫反应性的积聚。受损轴突可能有一种通过泛素介导的蛋白水解途径降解蛋白质的机制,以及另一种通过PGP 9.5的作用进行有效泛素再生循环的机制。

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