Effects of age and gender on Sirt 1 mRNA expressions in the hypothalamus of the mouse

Lafontaine-Lacasse, Mathieu; Richard, Denis; Picard, Frédéric

doi:10.1016/j.neulet.2010.01.008

Cited by 35 publications

(19 citation statements)

References 24 publications

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“…Previous studies showed that the expression of Sirt1 changed with aging (Alcendor et al, 2007;Ferrara et al, 2008). In brains, recent studies showed that Sirt1 expression was modified in specific areas of the brain in mice upon aging, and Sirt1 mRNA levels were strongly decreased upon aging in the hypothalamus (Lafontaine-Lacasse et al, 2010). However, other studies demonstrated that myocardial Sirt1 expression showed no difference between young and old rats (Cross et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Effect of breed on the expression of Sirtuins (Sirt1-7) and antioxidant capacity in porcine brain

Ren

Shan

Zhu

et al. 2013

Animal

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Sirtuins, NAD-dependent histone deacetylase (HDAC), are correlated to aging and antioxidant. The aim of this study was to determine breed differences of porcine Sirtuins expression and antioxidant capacity in brain between Jinhua pigs (a fatty breed of China) and Danish Landrace pigs (a leaner breed). Effect of age on Sirtuins' expression was also investigated. At the age of 180 days, the mRNA levels of Sirt1, as well as Sirt2 and Sirt4, in Jinhua pigs were greater, but the mRNA levels of Sirt3, Sirt5, Sirt6, and Sirt7 of Jinhua pigs were lower compared with Danish Landrace pigs. Likewise, at the same BW of 64 kg, the mRNA levels of Sirtuins, except Sirt5 and Sirt7, in Jinhua pigs were greater than Danish Landrace pigs. Meanwhile, Jinhua pigs possessed higher antioxidants activity than Danish Landrace pigs either at the same age or at the same BW. Furthermore, mRNA levels of Sirtuins were decreased with age in brain of the two breeds from 30 to 120 days. The results indicated that Sirtuins expression in brain was different between fatty and lean pigs, and Sirtuins expression may be correlated to antioxidant capacity. In addition, age could down-regulate Siruins expression in porcine brain.

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Section: Discussionmentioning

confidence: 99%

Effect of breed on the expression of Sirtuins (Sirt1-7) and antioxidant capacity in porcine brain

Ren

Shan

Zhu

et al. 2013

Animal

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“…The sirtuin family and specifically SIRT-1 are implicated in a majority of the physiological benefits of caloric restriction [203–205]. SIRT-1 expression decreases in a multitude of tissues with advancing age [206–208]. SIRT-1 function is related to deacetylation and thereby modulating activity of nuclear transcription factors, co-regulators and proteins to adapt gene expression in response to the cellular energy state and provide “stress resistance” by reducing pro-inflammatory and oxidative stress pathways [209].…”

Section: Energy Sensing Longevity Pathwaysmentioning

confidence: 99%

Cellular and molecular biology of aging endothelial cells

Donato

Morgan

Walker

et al. 2015

Journal of Molecular and Cellular Cardiology

401

365

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Cardiovascular disease (CVD) is the leading cause of death in the United States and aging is a major risk factor for CVD development. One of the major age-related arterial phenotypes thought to be responsible for the development of CVD in older adults is endothelial dysfunction. Endothelial function is modulated by traditional CVD risk factors in young adults, but advancing age is independently associated with the development of vascular endothelial dysfunction. This endothelial dysfunction results from a reduction in nitric oxide bioavailability downstream of endothelial oxidative stress and inflammation that can be further modulated by traditional CVD risk factors in older adults. Greater endothelial oxidative stress with aging is a result of augmented production from the intracellular enzymes NADPH oxidase and uncoupled eNOS, as well as from mitochondrial respiration in the absence of appropriate increases in antioxidant defenses as regulated by relevant transcription factors, such as FOXO. Interestingly, it appears that NFkB, a critical inflammatory transcription factor, is sensitive to this age-related endothelial redox change and its activation induces transcription of pro-inflammatory cytokines that can further suppress endothelial function, thus creating a vicious feed-forward cycle. This review will discuss the two macro-mechanistic processes, oxidative stress and inflammation, that contribute to endothelial dysfunction with advancing age as well as the cellular and molecular events that lead to the vicious cycle of inflammation and oxidative stress in the aged endothelium. Other potential mediators of this pro-inflammatory endothelial phenotype are increases in immune or senescent cells in the vasculature. Of note, genomic instability, telomere dysfunction or DNA damage have been shown to trigger cell senescence via the p53/p21 pathway that results in increased inflammatory signaling in arteries from older adults. This review will discuss the current state of knowledge regarding the emerging concepts of senescence and genomic instability as mechanisms underlying oxidative stress and inflammation in the aged endothelium. Lastly, energy sensitive/stress resistance pathways (SIRT-1, AMPK, mTOR) are altered in endothelial cells and/or arteries with aging and these pathways may modulate endothelial function via key oxidative stress and inflammation-related transcription factors. This review will also discuss what is known about the role of “energy sensing” longevity pathways in modulating endothelial function with advancing age. With the growing population of older adults, elucidating the cellular and molecular mechanisms of endothelial dysfunction with age is critical to establishing appropriate and measured strategies to utilize pharmacological and lifestyle interventions aimed at alleviating CVD risk.

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“…In response to DNA damage, SIRT1 relocates to DNA breaks to promote repair, resulting in transcriptional changes that parallel those observed in the aging mouse brain (Oberdoerffer et al, 2008). Although SIRT1 levels change with aging in various brain areas in mice (Lafontaine-Lacasse et al, 2010) the hippocampus was not analyzed in this study. Extrapolating from observations showing a preserved synaptogenic and functional activation potential of newborn GCs in the aging DG (Marrone et al, 2011) one would predict SIRT1 levels to be unaffected by aging in adult-born immature neurons of the SGZ.…”

Section: Small Non-coding Rnas In the Regulation Of Adult Hippocampalmentioning

confidence: 99%

New Neurons in Aging Brains: Molecular Control by Small Non-Coding RNAs

Schouten¹,

Buijink²,

Lucassen³

et al. 2012

Front. Neurosci.

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Adult neurogenesis generates functional neurons from neural stem cells present in specific brain regions. It is largely confined to two main regions: the subventricular zone of the lateral ventricle, and the subgranular zone of the dentate gyrus (DG), in the hippocampus. With age, the function of the hippocampus and particularly the DG is impaired. For instance, adult neurogenesis is decreased with aging, in both proliferating and differentiation of newborn cells, while in parallel an age-associated decline in cognitive performance is often seen. Surprisingly, the synaptogenic potential of adult-born neurons is only marginally influenced by aging. Therefore, although proliferation, differentiation, and synaptogenesis of adult-born new neurons in the DG are closely related to each other, they are differentially affected by aging. In this review we discuss the crucial roles of a novel class of recently discovered modulators of gene expression, the small non-coding RNAs, in the regulation of adult neurogenesis. Multiple small non-coding RNAs are differentially expressed in the hippocampus. In particular a subgroup of the small non-coding RNAs, the microRNAs, fine-tune the progression of adult neurogenesis. This makes small non-coding RNAs appealing candidates to orchestrate the functional alterations in adult neurogenesis and cognition associated with aging. Finally, we summarize observations that link changes in circulating levels of steroid hormones with alterations in adult neurogenesis, cognitive decline, and vulnerability to psychopathology in advanced age, and discuss a potential interplay between steroid hormone receptors and microRNAs in cognitive decline in aging individuals.

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Effects of age and gender on Sirt 1 mRNA expressions in the hypothalamus of the mouse

Cited by 35 publications

References 24 publications

Effect of breed on the expression of Sirtuins (Sirt1-7) and antioxidant capacity in porcine brain

Effect of breed on the expression of Sirtuins (Sirt1-7) and antioxidant capacity in porcine brain

Cellular and molecular biology of aging endothelial cells

New Neurons in Aging Brains: Molecular Control by Small Non-Coding RNAs

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