The ageing phenome: caloric restriction and hormones promote neural cell survival, growth, and de-differentiation

Timiras, Paola S.; Yaghmaie, F.; Saeed, Omar; Thung, Elaine; Chinn, Garrett M.

doi:10.1016/j.mad.2004.09.020

Cited by 8 publications

(5 citation statements)

References 48 publications

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“…In our study, curcumin upregulation of the histone 1 gene by at least twofold compared to controls, suggests that curcumin might, in fact, be involved in epigenetic modifications [41]. Indeed, the upregulation by curcumin of neurofilament M, reported here (Table 1) may support the hypothesis presented by recent studies that neuroglia cells, under the influence of growth factors, may de-differentiate into precursor cells that possibly may trans-differentiate into neuroblasts and neurons [41][42][43][44].…”

Section: Discussionsupporting

confidence: 88%

Early Anti-Oxidative and Anti-Proliferative Curcumin Effects on Neuroglioma Cells Suggest Therapeutic Targets

et al. 2008

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Curcumin (diferuloyl), from the Indian spice turmeric, reduces oxidative damage and induces apoptosis. Utilizing DNA microarrays, we have demonstrated that a low (5 microM) dose of curcumin added to a mixture of astrocytes and oligodendrocytes (C6 rat glioma cells) in culture for 24 and 48 h significantly modulates gene expression in four primary pathways: oxidative stress, cell cycle control, and DNA transcription and metabolism. Contribution of the pentose phosphate pathway to the pool of NADH upregulates glutathione and activates aldehyde oxidase. We have identified also several new genes, up- or downregulated by curcumin, namely, aldo-keto reductase, glucose-6-phosphate dehydrogenase, and aldehyde oxidase that protect against oxidative stress. The identification of several new cell cycle control genes, including the apoptosis-related protein (pirin) and insulin-like growth factor (IGF), and of the neurofilament M protein involved in neurogenesis suggests that curcumin may have applicability in the treatment of a spectrum of neurodegenerative diseases.

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Section: Discussionsupporting

confidence: 88%

Early Anti-Oxidative and Anti-Proliferative Curcumin Effects on Neuroglioma Cells Suggest Therapeutic Targets

et al. 2008

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“…Similarly, several studies also found that some injury including mechanical trauma, focal ischemia, kainate-iduced neuroexcitotoxicity etc., can induce ASTs residing close to injured zones of CNS to regain multipotent stem cell characteristics, and even to revert to initiative undifferentiated state (Chen et al 2005;Yu et al 2006;Steindler and Laywell 2003;Kaya et al 1999;Duggal et al 1997;Chang et al 2007). Additionally, some soluble factors produced by exogenous appropriate transplants such as embryonic neural tissues, neurons, and stem cells can also lead to re-expression of progenitor cells/ NSCs phenotype in ASTs (Leavitt et al 1999;Timiras et al 2005;Hunter and Hatten 1995;Schmid et al 2003). In agreement with in vivo data, there is still some in vitro evidence that ASTs can express a NSC/precursor cell identity when subjected to various appropriate molecular stimuli (Itoh et al 2006;Pillai et al 2006;Zhou et al 2001;Monnin et al 2007).…”

Section: Introductionmentioning

confidence: 79%

De-differentiation Response of Cultured Astrocytes to Injury Induced by Scratch or Conditioned Culture Medium of Scratch-Insulted Astrocytes

Yang

Cheng

et al. 2009

Cell Mol Neurobiol

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Our previous reports indicated that astrocytes (ASTs) in injured adult rat spinal cord underwent a process of de-differentiation, and may acquire the potential of neural stem cells (NSCs). However, the AST de-differentiation and transitional rejuvenation process following injury is still largely unclear. The aim of the present study was to determine whether injured in vitro ASTs can re-enter the multipotential-like stem cell pool and regain NSC characteristics, and to further understand the mechanism of AST de-differentiation. We used an in vitro scratch-wound model to evoke astrocytic response to mechanical injury. GFAP and nestin double-labeled indirect immunofluorescence were carried out to characterize these scratched cells at various periods. Western-blot analysis was used to determine the changes of GFAP and nestin expression following injury. Furthermore, the rate of proliferation was determined by immunocytochemical detection of BrdU incorporating cells. These scratch-wound ASTs were cultured with stem cells medium to explore their ability to generate neurospheres and examine the self-renewal and multi-potency of such neurospheres. Moreover, scratched AST culture supernatant as conditioned cultured medium (ACM) was used to investigate if some diffusible factors derived from injured ASTs could induce de-differentiation of AST. The results showed: (1) the nestin positivity first appeared in GFAP-positive cells at the edge of the scratch, subsequently, disseminated into un-insulted zone. The expression of nestin in AST was increased with longer culture, while that of GFAP was decreased. Furthermore, these nestin-immunoreactive ASTs could generate neurospheres, which showed self-renewal and could be differentiated into neurons, ASTs and oligodendrocytes. (2) Scratched ASTs culture supernatant can induce astrocytic proliferation and de-differentiation. These results reveal that the in vitro injured ASTs can de-differentiate into nestin-positive stem/precursor cells, the process of de-differentiation may arise from direct injury or some diffusible factors released from injured ASTs.

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“…In other words, the hormesis hypothesis embraces many of other proposed mechanisms, suggesting that while high intensity stress may trigger pathology and death, low intensities or concentrations of environmental challenges would lead to a beneficial change. Thus, under hormesis, DNA repair capacity would become a relevant mechanism where CR is capable of enhancing stress response genes such as DNA polymerase β, leading to resistance to stress and enhanced longevity ( 14 , 33 , 116 ).…”

Section: Introductionmentioning

confidence: 99%

Caloric restriction and genomic stability

Heydari

Unnikrishnan

Lucente

et al. 2007

Nucleic Acids Research

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Caloric restriction (CR) reduces the incidence and progression of spontaneous and induced tumors in laboratory rodents while increasing mean and maximum life spans. It has been suggested that CR extends longevity and reduces age-related pathologies by reducing the levels of DNA damage and mutations that accumulate with age. This hypothesis is attractive because the integrity of the genome is essential to a cell/organism and because it is supported by observations that both cancer and immunological defects, which increase significantly with age and are delayed by CR, are associated with changes in DNA damage and/or DNA repair. Over the last three decades, numerous laboratories have examined the effects of CR on the integrity of the genome and the ability of cells to repair DNA. The majority of studies performed indicate that the age-related increase in oxidative damage to DNA is significantly reduced by CR. Early studies suggest that CR reduces DNA damage by enhancing DNA repair. With the advent of genomic technology and our increased understanding of specific repair pathways, CR has been shown to have a significant effect on major DNA repair pathways, such as NER, BER and double-strand break repair.

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The ageing phenome: caloric restriction and hormones promote neural cell survival, growth, and de-differentiation

Cited by 8 publications

References 48 publications

Early Anti-Oxidative and Anti-Proliferative Curcumin Effects on Neuroglioma Cells Suggest Therapeutic Targets

Early Anti-Oxidative and Anti-Proliferative Curcumin Effects on Neuroglioma Cells Suggest Therapeutic Targets

De-differentiation Response of Cultured Astrocytes to Injury Induced by Scratch or Conditioned Culture Medium of Scratch-Insulted Astrocytes

Caloric restriction and genomic stability

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