Premium
Expression of the ubiquitin carboxyl‐terminal hydrolase PGP 9.5 in axons following spinal cord compression trauma. An immunohistochemical study in the rat
Author(s) -
LI GUI LIN,
FAROOQUE MOHAMMAD,
HOLTZ ANDERS,
OLSSON YNGVE
Publication year - 1997
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1997.tb00585.x
Subject(s) - spinal cord , ubiquitin , axoplasmic transport , immunohistochemistry , proteolysis , axon , microbiology and biotechnology , neuron , biology , chemistry , anatomy , neuroscience , biochemistry , enzyme , gene , immunology
Protein gene product 9.5 (PGP 9.5) is a neuron‐specific protein which acts as a ubiquitin carboxylterminal 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.