Tau Isoforms Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Usarek, Ewa; Kuźma‐Kozakiewicz, Magdalena; Schwalenstöcker, Birgit; Kaźmierczak, Beata; Münch, Christoph; Ludolph, Albert C.; Barańczyk‐Kuźma, Anna

doi:10.1007/s11064-006-9057-3

Cited by 7 publications

(14 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The present work is a continuation of our previous studies [10] in which we indicated changes in tau isoforms expression in frontal cortex and hippocampus, but not in the spinal cord of transgenic adult mice harboring human SOD1 with G93A amyotrophic lateral sclerosis-associated mutation, at presymptomatic and symptomatic stage of ALS (age 64 and 120 days, respectively). We confirmed the earlier results with the use of Northern blotting.…”

Section: Introductionsupporting

confidence: 69%

“…Reverse transcription reaction, as well as the analysis of alternative splicing of exons 2, 3 (N-terminal part of tau protein) and 10 (C-terminal part) were performed as described earlier [10]. The expression of tau-mRNA isoforms was determined semi-quantitatively and expressed as the ratio of optical density band of tau isoform to optical density of 40 S ribosomal S12 protein RNA (housekeeping gene) as described earlier [10].…”

Section: Rt-pcrmentioning

confidence: 99%

“…Electrophoresis in 16% polyacrylamide gel (SDS-PAGE) was run according to Laemmli [13]. Immunoblotting was performed using with polyclonal anti-tau-1 primary antibodies, as described earlier [10].…”

Section: Western Blottingmentioning

confidence: 99%

See 2 more Smart Citations

Age-related Changes in Tau Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

et al. 2007

Self Cite

View full text Add to dashboard Cite

The work is a continuation of studies on tau expression and alternative splicing in the central nervous system of transgenic mice harboring human SOD1 with G93A amyotrophic lateral sclerosis (ALS)-associated mutation. Since age is an important risk factor for ALS, we expanded the studies into younger animals (age 5 and 25 days). We also included cerebellum, a structure not studied in the context of neurodegeneration in ALS. We found decreased total tau-mRNA expression in hippocampus but not in cortex and spinal cord of young transgenics, and a lack of exon 10 in 5-day-old mice. In cerebellum, the total tau-mRNA expression was increased in transgenic animals during the whole period of life, however at the symptomatic stage of ALS (age 120 days) the level of protein was decreased. It can be concluded that the SOD1 G93A mutation causes early alterations of tau expression in cns, which are not exclusively restricted to the upper and lower motor neuron.

show abstract

Section: Introductionsupporting

confidence: 69%

Section: Rt-pcrmentioning

confidence: 99%

See 1 more Smart Citation

Age-related Changes in Tau Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

et al. 2007

Self Cite

View full text Add to dashboard Cite

show abstract

“…The N-terminal part of tau is also crucial for the determination of spacing between microtubules [33,34]. As we have shown, the N-terminal but not the C-terminal part of tau is affected in the SOD1G93A mice [28,35]. LaPointe et al [36] indicated that the first 18 amino acids at the N terminus of squid axoplasm tau are required to elicit the inhibitory effect of tau filaments on kinesin-dependent fast axonal anterograde transport.…”

Section: Discussionmentioning

confidence: 99%

Kinesin Expression in the Central Nervous System of Humans and Transgenic hSOD1G93A<b> </b>Mice with Amyotrophic Lateral Sclerosis

Kuźma‐Kozakiewicz

Chudy²,

Gajewska³

et al. 2012

Neurodegener Dis

Self Cite

View full text Add to dashboard Cite

Background: Amyotrophic lateral sclerosis is a fatal motor neuron degenerative disease. Most cases are sporadic (SALS), and approximately 10% are familial (FALS) among which over 20% are linked to the SOD1 mutation. Both SALS and FALS have been associated with retrograde axonal transport defects. Kinesins (KIFs) are motor proteins involved mainly in anterograde transport; however, some also participate in retrograde transport. Objective: The purpose of the study was to investigate and compare the expression of kinesins involved in anterograde (KIF5A, 5C) and retrograde (KIFC3/C2) axonal transport in SALS in humans and FALS in mice with the hSOD1G93A mutation. Methods: The studies were conducted on various parts of the CNS from autopsy specimens of SALS patients, and transgenic mice at presymptomatic and symptomatic stages using real-time quantitative PCR and reverse-transcription PCR. Results: All KIF expression in the motor cortex of individual SALS subjects was higher than in the adjacent sensory cortex, in contrast to the expression in control brains. It was also significantly higher in the frontal cortex of symptomatic but not presymptomatic mice compared to wild-type controls. However, the mean KIF expression in the SALS motor and sensory cortexes was lower than in control cortexes. To a lesser extent the decrease in KIF mean expression also occurred in human but not in mouse ALS spinal cords and in both human and mouse cerebella. Conclusion: Disturbances in kinesin expression in the CNS may dysregulate both anterograde and retrograde axonal transports leading to motor neuron degeneration.

show abstract

“…Details of this relative quantification can be found at http://docs.appliedbiosystems.com/pebiodocs/04303859.pdf. All quantifications were normalized to an established internal control for rodent brain (ribosomal S12 protein RNA, housekeeping gene), which was coamplified as described previously by others (Heinrich et al, 2006;Usarek et al, 2006;Nanda et al, 2008). For each group the results were given as mean 6 SEM.…”

Section: Real-time Quantitative Rt-pcrmentioning

confidence: 99%

Early life stress stimulates hippocampal reelin gene expression in a sex‐specific manner: Evidence for corticosterone‐mediated action

et al. 2010

View full text Add to dashboard Cite

ABSTRACT:Early life stress predisposes to the development of psychiatric disorders. In this context the hippocampal formation is of particular interest, because it is affected by stress on the structural and cognitive level. Since little is known how early life stress is translated on the molecular level, we mimicked early life stress in mouse models and analyzed the expression of the glycoprotein Reelin, a master molecule for development and differentiation of the hippocampus. From postnatal day 1 (P1) to P14, mouse pups were subjected to one of the following treatments: nonhandling (NH), handling (H), maternal separation (MS), and early deprivation (ED) followed by immediate (P15) or delayed (P70) real time RT-PCR analysis of reelin mRNA expression. We show that at P15, reelin mRNA levels were significantly increased in male H and ED groups when compared with the NH group. In contrast, no stress-induced alterations of reelin mRNA expression were found in female animals. This sex difference in stress-mediated stimulation of reelin expression was maintained into adulthood, since at P70 intergroup differences were still found in male, but not in female mice. On the cellular level, however, we did not find any significant differences in cell densities of Reelin-immunolabeled neurons between treatment groups or sexes, but an overall reduction of Reelin-expressing neurons in the adult hippocampus when compared to P15. To address the question whether corticosterone mediates the stress-induced up-regulation of reelin gene expression, we used age-matched hippocampal slice cultures derived from male and female mouse pups. Quantitative determination of mRNA levels revealed that corticosterone treatment significantly up-regulated reelin mRNA expression in male, but not in female hippocampi. Taken together, these results show a sex-specific regulation of reelin gene expression by early life experience, most likely mediated by corticosterone. V V C 2010 Wiley-Liss, Inc.

show abstract

Tau Isoforms Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Cited by 7 publications

References 33 publications

Age-related Changes in Tau Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Age-related Changes in Tau Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Kinesin Expression in the Central Nervous System of Humans and Transgenic hSOD1G93A<b> </b>Mice with Amyotrophic Lateral Sclerosis

Early life stress stimulates hippocampal reelin gene expression in a sex‐specific manner: Evidence for corticosterone‐mediated action

Contact Info

Product

Resources

About