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

Kaźmierczak, Beata; Kuźma‐Kozakiewicz, Magdalena; Usarek, Ewa; Barańczyk‐Kuźma, Anna

doi:10.18388/abp.2011_2233

Cited by 6 publications

(6 citation statements)

References 48 publications

(51 reference statements)

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“…The disturbances of tau expression, especially in the frontal cortex and cerebellum, were more severe in mice with the SOD1G93A than with the Dync1h1 mutation (Kuźma-Kozakiewicz et al, 2011). Studying glutathione S-transferase pi, an enzyme involved in detoxification of electrophilic compounds and products of oxidative stress, we found that its expression was decreased in the frontal cortex, hippocampus and spinal cord of SOD1/+ but not Cra1/+ mice (Kaźmierczak et al, 2011). Dissimilarities between the two models have also been seen by other groups.…”

Section: Discussionmentioning

confidence: 82%

“…We performed studies on brain frontal cortex and cervical spinal cord, the structures usually affected in ALS, and on the hippocampus, a structure not affected (control) by the disease. We also included the cerebellum, the CNS structure rarely studied in motor neuron degeneration (MND), because of a number of interesting features we had observed there previously (Barańczyk-Kuźma et al, 2007;Kaźmierczak et al, 2011;Kuźma-Kozakiewicz et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2013

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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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Section: Discussionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

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

et al. 2013

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“…GSTP1 is characterized as a single subclass of GSTs involved with cellular protection against oxidative stress elements in the central nervous system, acting in the inhibition of oxidative damage to proteins, lipids, and nucleic acids [ 15 , 43 ]. Reduced levels of GSTP1 messenger RNA (mRNA) have been already observed in mice transgenic for SODG93A, an animal model of ALS [ 43 ]. In analysis of protein and mRNA expression of peripheral blood mononuclear cells from ALS patients had been showed reduced expression of GSTP1 [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

No association of GSTP1 rs1695 polymorphism with amyotrophic lateral sclerosis: A case-control study in the Brazilian population

et al. 2021

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Amyotrophic Lateral Sclerosis (ALS) is a rare neurodegenerative disease that affects motor neurons and promotes progressive muscle atrophy. It has a multifactorial etiology, where environmental conditions playing a remarkable role through the increase of oxidative stress. Genetic polymorphisms in cell detoxification genes, such as Glutathione S-Transferase Pi 1 (GSTP1) can contribute to excessive oxidative stress, and therefore may be a risk factor to ALS. Thus, this study aimed to investigate the role of the GSTP1 rs1695 polymorphism in ALS susceptibility in different genetic inheritance models and evaluate the association of the genotypes with risk factors, clinical and demographic characteristics of ALS patients from the Brazilian central population. This case-control study was conducted with 101 patients with ALS and 101 healthy controls. GSTP1 rs1695 polymorphism genotyping was performed with Polymerase Chain Reaction–Restriction Fragment Length Polymorphism (PCR-RFLP). The statistical analysis was carried out using the SPSS statistical package and SNPStats software. Analysis of genetic inheritance models was performed by logistic regression, which was used to determine the Odds Ratio. The results of this first study in the Brazilian population demonstrated that there was no risk association between the development of ALS and the GSTP1 rs1695 polymorphism in any genetic inheritance model (codominant, dominant, recessive, overdominant, and logarithmic); and that the polymorphic variants were not associated with the clinical and demographic characteristics of ALS patients. No association of the GSTP1 rs1695 polymorphism and ALS development in the Brazilian central population was found. These findings may be justified by the multifactorial character of the disease.

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“…At a pre-symptomatic age (70 days), expression of this protein was unchanged, but it was decreased at a symptomatic age (140 days) in SOD1 mice, but not in Cra1/SOD1 mice. Expression of this protein was stable in the spinal cord of Cra1 mutant mice when compared with WT mice [67]; the authors conclude that the DYNC1H1 mutation reduces the toxic effects caused by the SOD1 mutation in Cra1/SOD1 mice. Because of the similarity of Loa and Cra1 mutations, it is possible that Loa/+ mice also have a normal level of expression of GST pi.…”

Section: Discussionmentioning

confidence: 99%

Morphological changes and altered expression of antioxidant proteins in a heterozygous dynein mutant; a mouse model of spinal muscular atrophy

Wiggins

2014

Oxid Antioxid Med Sci

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Objective There is increased evidence that oxidative stress is involved in exacerbations of neurodegenerative diseases and spinal muscular atrophies. Methods We examined changes in morphology and expression of antioxidant proteins and peroxiredoxins in motor neurons of lumbar spinal cord, dorsal root ganglion sensory neurons, macroglial cells and quadriceps muscles of newborn heterozygous Loa/+ mice (“legs at odd angles”), a mouse model for early onset of the spinal muscular atrophy with lower extremity predominance (SMA-LED). Results Our data indicate that newborn Loa-mice develop: neuroinflammation of the sensory and motor neurons; muscular inflammation with atrophic and denervated myofibers; increased expression of neuronal mitochondrial peroxiredoxins (Prxs) 3, 5 and cytoplasmic Prx 6 in motor and sensory neurons, myofibers, fibroblasts of perimysium and chondrocytes of cartilage; and decreased expression of Prx 6 by glial cells and in extracellular space surrounding motor neurons. Conclusion The decrease in expression of Prx 6 by glial cells and extracellular Prx 6 secretion in early stages of the pathological conditions is consistent with the hypothesis that chronic oxidative stress may lead to neurodegeneration of motor neurons and exacerbation of the pathology.

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

Cited by 6 publications

References 48 publications

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

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

No association of GSTP1 rs1695 polymorphism with amyotrophic lateral sclerosis: A case-control study in the Brazilian population

Morphological changes and altered expression of antioxidant proteins in a heterozygous dynein mutant; a mouse model of spinal muscular atrophy

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