c-Myb Immunoreactivity, Protein and mRNA Levels Significantly Increase in the Aged Hippocampus Proper in Gerbils

Hwang, In Koo; Moon, Soo-Mook; Yoo, Ki‐Yeon; Li, Hua; Kwon, Heum Dai; Hwang, Ho Sik; Choi, Sun Ok; Lee, Bong-Hee; Kim, Jong Dai; Won, Moo Ho

doi:10.1007/s11064-006-9278-5

Cited by 12 publications

(13 citation statements)

References 21 publications

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“…Furthermore, inflammation appears to play a central role among the various processes that have been associated with brain aging. Moreover, the hippocampus is a brain region essential for intact cognitive abilities and appears to be particularly vulnerable to the aging process [14][15][16][17][18]. Dogs are known to develop a well characterized cognitive deficit syndrome during aging [19][20][21], and age-related changes are observed in the canine brain which is accepted as a model of human brain aging [19,[21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Comparison of Ionized Calcium-binding Adapter Molecule 1 Immunoreactivity of the Hippocampal Dentate Gyrus and CA1 Region in Adult and Aged Dogs

Hwang

Lee

et al. 2008

Neurochem Res

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Similarities between age-related changes in the canine and human brain have resulted in the general acceptance of the canine brain as a model of human brain aging. The hippocampus is essentially required for intact cognitive ability and appears to be particularly vulnerable to the aging process. We observed changes in ionized calcium-binding adapter molecule 1 (Iba-1, a microglial marker) immunoreactivity and protein levels in the hippocampal dentate gyrus and CA1 region of adult (2-3 years) and aged (10-12 years) dogs. We also observed the interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, protein levels in these groups. In the dentate gyrus and CA1 region of the adult dog, Iba-1 immunoreactive microglia were well distributed and their processes were highly ramified. However, in the aged dog, the processes of Iba-1 immunoreactive microglia were hypertrophied in the dentate gyrus. Moreover, Iba-1 protein level in the dentate gyrus in the aged dog was higher than in the adult dog. IFN-gamma expression was increased in the dentate gyrus homogenates of aged dogs than adult dogs. In addition, we found that some neurons were positive to Fluoro-Jade B (a marker for neuronal degeneration) in the dentate polymorphic layer, but not in the hippocampal CA1 region in the aged dog. These results suggest that Iba-1 immunoreactive microglia are hypertrophied in the dentate gyrus in the aged dog.

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Section: Introductionmentioning

confidence: 99%

Comparison of Ionized Calcium-binding Adapter Molecule 1 Immunoreactivity of the Hippocampal Dentate Gyrus and CA1 Region in Adult and Aged Dogs

Hwang

Lee

et al. 2008

Neurochem Res

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“…In particular, HSF3 induces the expression of Hsps by binding to c-myb (Tanikawa et al 2001). Recently, it was reported that the c-myb protein and mRNA were increased during the Gerbil hippocampus ageing process (Hwang et al 2007). These phenomena may suggest that elevation of c-myb expression serves anti-apoptosis role in aged cells.…”

Section: Discussionmentioning

confidence: 99%

“…However, a recent study reported that c-myb increases the protein level during ageing (Hwang et al 2007). This study examined the role of c-myb in cell survival against oxidative stress in aged HDF cells.…”

Section: Introductionmentioning

confidence: 99%

c-myb has a character of oxidative stress resistance in aged human diploid fibroblasts: regulates SAPK/JNK and Hsp60 pathway consequently

Lee

Bhattarai

et al. 2009

Biogerontology

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This study examined whether c-myb acts as a survival molecule in aged cells. A previous in vitro ageing model suggested that aged cells have a higher cell capacity for survival after exposure to oxidative stress, which involves blockage of the translocation of Hsp60 from the mitochondria to the cytoplasm followed by SAPK/JNK inactivation, than young cells. In human diploid fibroblasts (HDFs), c-myb expression increased gradually with ageing, and this increase had a significant influence on the cell survival capacity after exposure to oxidative stress. To clarify the role of c-myb in oxidative stress, young cells under 21 passages, which lacked c-myb expression, were transfected with adenovirus-mediated c-myb for express c-myb. These c-myb-over-expressed young cells showed increased cell viability upon exposure to oxidative stress to a similar extent to that of the aged cells. In addition, these c-myb-over-expressed young cells did not exhibit SAPK/JNK activation, Hsp60 displacement and cytochrome C release, as was observed in aged cells. The aged cells that had c-myb suppressed using siRNA c-myb showed reduced cell viability and increased apoptosis in a manner to that observed in young cells. From this study, c-myb blocked SAPK/JNK and Hsp60 translocation upon exposure to oxidative stress. This result suggests that c-myb might act as a modulator of cell survival in the ageing process by suppressing apoptosis in aged cells.

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“…In addition to these findings, the researchers discovered that many of the promoters of differentially methylated genes were enriched with binding sites of transcription factor MYB in samples of patients without known mutations. Interestingly, this transcription factor has been linked to aging [142], as well as to the response to oxidative stress of aged cells [143]. …”

Section: Link To Diseasementioning

confidence: 99%

Causes and Consequences of Age-Related Changes in DNA Methylation: A Role for ROS?

Rang¹,

Boonstra

2014

Biology

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Recent genome-wide analysis of C-phosphate-G (CpG) sites has shown that the DNA methylome changes with increasing age, giving rise to genome-wide hypomethylation with site‑specific incidences of hypermethylation. This notion has received a lot of attention, as it potentially explains why aged organisms generally have a higher risk of age-related diseases. However, very little is known about the mechanisms that could cause the occurrence of these changes. Moreover, there does not appear to be a clear link between popular theories of aging and alterations in the methylome. Some of the most fruitful of these theories attribute an important role to reactive oxygen species, which seem to be responsible for an increase in oxidative damage to macromolecules, such as DNA, during the lifetime of an organism. In this review, the connection between changes in DNA methylation and these reactive oxygen species is discussed, as well as the effect of these changes on health. Deeper insights into the nature, causes and consequences of the aging methylome might provide a deeper understanding of the molecular mechanisms of aging and eventually contribute to the development of new diagnostic and therapeutic tools.

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c-Myb Immunoreactivity, Protein and mRNA Levels Significantly Increase in the Aged Hippocampus Proper in Gerbils

Cited by 12 publications

References 21 publications

Comparison of Ionized Calcium-binding Adapter Molecule 1 Immunoreactivity of the Hippocampal Dentate Gyrus and CA1 Region in Adult and Aged Dogs

Comparison of Ionized Calcium-binding Adapter Molecule 1 Immunoreactivity of the Hippocampal Dentate Gyrus and CA1 Region in Adult and Aged Dogs

c-myb has a character of oxidative stress resistance in aged human diploid fibroblasts: regulates SAPK/JNK and Hsp60 pathway consequently

Causes and Consequences of Age-Related Changes in DNA Methylation: A Role for ROS?

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