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1

Ekspresja transferazy S-glutationowej pi w transgenicznych mysich modelach neurodegeneracji

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Kazmierczak B., Usarek E., Kuzma-Kozakiewicz M., Baranczyk-Kuzma A.
Medycyna Weterynaryjna
|
2008
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tom 64
|
nr 06
812-814
Glutathione S-transferase pi (GST pi) inactivates a large variety of toxic, electrophilic compounds. The substrates of GST pi include environmental toxins and intracellular reactive oxygen species, factors significant in the pathogenesis of neurodegenerative diseases. The aim of the present study was to investigate the expression of glutathione S-transferase pi in transgenic mouse models of neurodegeneration on both the mRNA and protein levels. Experiments were conducted on the frontal cortex of transgenic B6-C3H hybrids SOD1, Cra1 and SOD1/Cra1, aged 70 and 140 days. The SOD1 mice express a human SOD1ᴳ⁹³ᴬ mutation, the Cra1 strain carries mutation in the cytoplasmic dynein heavy chain 1 (Dnchc1), and the double heterozygote SOD1/Cra1 mice show a delayed disease progression as well as an increased lifespan compared with the SOD1 strain. A wild strain of mice were used as a control. The expression of GST pi mRNA in younger mice (age 70 days) was found to be similar in all studied groups of animals. In older (aged 140 days) controls and Cra1 mice the GST pi expression was at a similar level and it did not significantly differ from younger animals. In SOD1 and SOD1/Cra1 strains, the mRNA-GST pi expression was lower when compared to 140-day-old controls and the Cra1 strain. Moreover, it was significantly lower than in corresponding 70-day-old animals. A decrease in the GST pi expression on the mRNA level was accompanied by a decrease in the protein level. High and unchanged GST pi expression in the frontal cortex of Cra1 mice indicates that the antioxidant-detoxification system plays an important role in protection against neurodegeneration. A significant decrease of GST pi expression in the frontal cortex of SOD1 and SOD1/Cra1 mice at the symptomatic stage of the disease suggests that the expression of this enzyme is related more to the G93A mutation in the SOD1 gene than to the efficient axonal transport.
2

Differences in glutathione S-transferase pi expression in transgenic mice with symptoms of neurodegeneration

100%
Kazmierczak B., Kuzma-Kozakiewicz M., Usarek E., Baranczyk-Kuzma A.
Acta Biochimica Polonica
|
2011
|
tom 58
|
nr 4
Glutathione S-transferase pi (GST pi) is an enzyme involved in cell protection against toxic electrophiles and products of oxidative stress. GST pi expression was studied in transgenic mice hybrids (B6-C3H) with symptoms of neurodegeneration harboring SOD1G93A (SOD1/+), Dync1h1 (Cra1/+) and double (Cra1/SOD1) mutations, at presymptomatic and symptomatic stages (age 70, 140, 365 days) using RT-PCR and Western blotting. The main changes in GST pi expression were observed in mice with the SODG93A mutation. In SOD1/+ and Cra1/SOD1 transgenics, with the exception of cerebellum, the changes in GST pi-mRNA accompanied those in GST pi protein. In brain cortex of both groups the expression was unchanged at the presymptomatic (age 70 days) but was lower at the symptomatic stage (age 140 days) and at both stages in hippocampus and spinal cord of SOD1/+ but not of Cra1/SOD1 mice compared to age-matched wild-type controls. In cerebellum of the presymptomatic and the symptomatic SOD1/+ mice and presymptomatic Cra1/SOD1 mice, the GST pi-mRNA was drastically elevated but the protein level remained unchanged. In Cra1/+ transgenics there were no changes in GST pi expression in any CNS region both on the mRNA and on the protein level. It can be concluded that the SOD1G93A but not the Dync1h1 mutation significantly decreases detoxification efficiency of GST pi in CNS, however the Dync1h1 mutation reduces the effects caused by the SOD1G93A mutation. Despite similarities in neurological symptoms, the differences in GST pi expression between SOD1/+ and Cra1/+ transgenics indicate a distinct pathogenic entity of these two conditions.
3

Changes in kinesin expression in the CNS of mice with dynein heavy chain 1 mutation

100%
Kuzma-Kozakiewicz M., Kazmierczak B., Usarek E., Baranczyk-Kuzma A.
Acta Biochimica Polonica
|
2013
|
tom 60
|
nr 1
 Dysfunction of fast axonal transport, vital for motor neurons, may lead to neurodegeneration. Anterograde transport is mediated by N-kinesins (KIFs), while retrograde transport by dynein 1 and, to a minor extent, by C-kinesins. In our earlier studies we observed changes in expression of N- and C-kinesins (KIF5A, 5C, C2) in G93ASOD1-linked mouse model of motor neuron degeneration. In the present work we analyze the profile of expression of the same kinesins in mice with a dynein 1 heavy chain mutation (Dync1h1, called Cra1), presenting similar clinical symptoms, and in Cra1/SOD1 mice with milder disease progression than SOD1 transgenics. We found significantly higher levels of mRNA for KIF5A and KIF5C but not the KIFC2 in the frontal cortex of symptomatic Cra1/+ mice (aged 365 days) compared to the wild-type controls. No changes in kinesin expression were found in the spinal cord of any age group and only mild changes in the hippocampus. The expression of kinesins in the cerebellum of the presymptomatic and symptomatic mice (aged 140 and 365 days, respectively) was much lower than in age-matched controls. In Cra1/SOD1 mice the changes in KIFs expression were similar or more severe than in the Cra1/+ groups, and they also appeared in the spinal cord. Thus, in mice with the Dync1h1 mutation, which impairs dynein 1-dependent retrograde transport, expression of kinesin mRNA is affected in various structures of the CNS and the changes are similar or milder than in mice with double Dync1h1/hSOD1G93A mutations.
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