Ekspresja transferazy S-glutationowej pi w transgenicznych mysich modelach neurodegeneracji

• Autorzy: Kazmierczak B , Usarek E. , Kuzma-Kozakiewicz M. , Baranczyk-Kuzma A.

Warianty tytułu

EN

Expression of glutathione S-transferase pi in transgenic mouse models of neurodegeneration

• Języki publikacji: PL

Abstrakty

EN

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.

Słowa kluczowe

PL

modele zwierzece; myszy transgeniczne; choroby neurodegeneracyjne; stwardnienie zanikowe boczne; neurodegeneracja; kora mozgowa; transferaza S-glutationowa pi; ekspresja bialek

• Wydawca: -
• Czasopismo: Medycyna Weterynaryjna
• Rocznik: 2008
• Tom: 64
• Numer: 06
• Opis fizyczny: s.812-814,rys.,fot.,bibliogr.

Twórcy

autor

Kazmierczak B

• Akademia Medyczna w Warszawie, ul.Banacha 1, 02-097 Warszawa

autor

Usarek E.

autor

Kuzma-Kozakiewicz M.

autor

Baranczyk-Kuzma A.

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