Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging

Hyun, Dong Hoon; Emerson, Scott S.; Jo, Dong Gyu; Mattson, Mark P.; Cabo, Rafael de

doi:10.1073/pnas.0608008103

Cited by 249 publications

(175 citation statements)

References 60 publications

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“…Several articles, published in the recent years, draw attention to the role CoQ 10 as cellular prooxidant, which plays a role in ROS signaling (Hyun et al, 2006;Linnane and Eastwood, 2006;Wang and Quinn, 1999). Therefore, in the context of results described here, that is, a relatively low dose of CoQ 10 producing full neuroprotection and causing the upregulation of astrocytic GFAP-immunoreactivity, other facets of CoQ 10 function should be also considered.…”

Section: Discussionmentioning

confidence: 96%

“…Thus, CoQ 10 which is present in most cellular membranes as a fundamental component of oxidoreductase systems can also be a source of superoxide and, consequently, hydrogen peroxide. They are generated by auto-oxidation of ubisemiquinone, an intermediate radical of ubiquinone and/or quinol oxidoreduction cycle (Abramov et al, 2005;Hyun et al, 2006;Liu et al, 2005;Ushio-Fukai, 2006;Wright and Kuhn, 2002). Until recently, superoxide and hydrogen peroxide have been regarded, mainly, as harmful byproducts of mitochondrial respiration and targeted by various antioxidant-based strategies to control neurodegeneration.…”

Section: Discussionmentioning

confidence: 99%

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Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

Sikorska

Lanthier

Miller

et al. 2014

Neurobiology of Aging

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Although the support for the use of antioxidants, such as coenzyme Q 10 (CoQ 10 ), to treat Parkinson's disease (PD) comes from the extensive scientific evidence, the results of conducted thus far clinical trials are inconclusive. It is assumed that the efficacy of CoQ 10 is hindered by insolubility, poor bioavailability, and lack of brain penetration. We have developed a nanomicellar formulation of CoQ 10 (Ubisol-Q 10 ) with improved properties, including the brain penetration, and tested its effectiveness in mouse MPTP (1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine) model with the objectives to assess its potential use as an adjuvant therapy for PD. We used a subchronic MPTP model (5-daily MPTP injections), characterized by 50% loss of dopamine neurons over a period of 28 days. Ubisol-Q 10 was delivered in drinking water. Prophylactic application of Ubisol-Q 10 , started 2 weeks before the MPTP exposure, significantly offset the neurotoxicity (approximately 50% neurons died in MPTP group vs. 17% in MPTP+ Ubisol-Q 10 group by day 28). Therapeutic application of Ubisol-Q 10 , given after the last MPTP injection, was equally effective. At the time of intervention on day 5 nearly 25% of dopamine neurons were already lost, but the treatment saved the remaining 25% of cells, which otherwise would have died by day 28. This was confirmed by cell counts, analyses of striatal dopamine levels, and improved animals' motor skill on a beam walk test. Similar levels of neuroprotection were obtained with 3 different Ubisol-Q 10 concentrations tested, that is, 30 mg, 6 mg, or 3 mg CoQ 10 /kg body weight/day, showing clearly that high doses of CoQ 10 were not required to deliver these effects. Furthermore, the Ubisol-Q 10 treatments brought about a robust astrocytic activation in the brain parenchyma, indicating that astroglia played an active role in this neuroprotection. Thus, we have shown for the first time that Ubisol-Q 10 was capable of halting the neurodegeneration already in progress;

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

Sikorska

Lanthier

Miller

et al. 2014

Neurobiology of Aging

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“…In contrast to temporally restricted feeding paradigms, which do not reduce calorie intake and which allow enough food to be eaten daily, hypocaloric feeding is known to lead to several beneficial physiological actions, such as slowing of ageing, extended lifespan and delayed onset of major age-related diseases in a number of species, including rodents and primates (Hyun et al, 2006;Wolf, 2006). In mice under a light-dark cycle, a daily hypocaloric feeding (i.e., 66% of animal's daily food intake given each day at the same time), but not temporally restricted feeding, leads to phase advances of behavioral and physiological circadian rhythms controlled by the SCN, whatever the feeding time over the daily cycle (Challet et al, 1998;Mendoza et al, 2005b).…”

Section: Animals and Housingmentioning

confidence: 99%

Forebrain oscillators ticking with different clock hands

Feillet

Mendoza

Albrecht

et al. 2008

Molecular and Cellular Neuroscience

134

113

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Clock proteins like PER1 and PER2 are expressed in the brain, but little is known about their functionality outside the main suprachiasmatic clock. Here we show that PER1 and PER2 were neither uniformly present nor identically phased in forebrain structures of mice fed ad libitum. Altered expression of the clock gene Cry1 was observed in respective Per1 or Per2 mutants. In response to hypocaloric feeding, PERs timing was not markedly affected in few forebrain structures (hippocampus). In most other forebrain oscillators, including those expressing only PER1 (e.g., dorsomedial hypothalamus), PER2 (e.g., paraventricular hypothalamus) or both (e.g., paraventricular thalamus), PER1 was up-regulated and PER2 largely phase-advanced. Cry1 expression was selectively modified in the forebrain of Per mutants challenged with hypocaloric feeding. Our results suggest that there is not one single cerebral clock, but a system of multiple brain oscillators ticking with different clock hands and differentially sensitive to nutritional cues.

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“…Male Fischer 344 (F344) rats were fed ad libitum (AL) or maintained on a 40% calorie restriction (CR) regimen beginning at 1 month of age as described 16, 17. The AL diet was the NIH‐31 standard diet, and the CR diet was a vitamin‐ and mineral‐fortified version of the NIH‐31, 40% less (by weight) than the average AL consumption.…”

Section: Methodsmentioning

confidence: 99%

Calorie Restriction Curbs Proinflammation That Accompanies Arterial Aging, Preserving a Youthful Phenotype

Wang

Zhang

Zhu

et al. 2018

JAHA

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BackgroundAging exponentially increases the incidence of morbidity and mortality of quintessential cardiovascular disease mainly due to arterial proinflammatory shifts at the molecular, cellular, and tissue levels within the arterial wall. Calorie restriction (CR) in rats improves arterial function and extends both health span and life span. How CR affects the proinflammatory landscape of molecular, cellular, and tissue phenotypic shifts within the arterial wall in rats, however, remains to be elucidated.Methods and ResultsAortae were harvested from young (6‐month‐old) and old (24‐month‐old) Fischer 344 rats, fed ad libitum and a second group maintained on a 40% CR beginning at 1 month of age. Histopathologic and morphometric analysis of the arterial wall demonstrated that CR markedly reduced age‐associated intimal medial thickening, collagen deposition, and elastin fractionation/degradation within the arterial walls. Immunostaining/blotting showed that CR effectively prevented an age‐associated increase in the density of platelet‐derived growth factor, matrix metalloproteinase type II activity, and transforming growth factor beta 1 and its downstream signaling molecules, phospho‐mothers against decapentaplegic homolog‐2/3 (p‐SMAD‐2/3) in the arterial wall. In early passage cultured vascular smooth muscle cells isolated from AL and CR rat aortae, CR alleviated the age‐associated vascular smooth muscle cell phenotypic shifts, profibrogenic signaling, and migration/proliferation in response to platelet‐derived growth factor.Conclusions CR reduces matrix and cellular proinflammation associated with aging that occurs within the aortic wall and that are attributable to platelet‐derived growth factor signaling. Thus, CR reduces the platelet‐derived growth factor–associated signaling cascade, contributing to the postponement of biological aging and preservation of a more youthful aortic wall phenotype.

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Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging

Cited by 249 publications

References 60 publications

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

Forebrain oscillators ticking with different clock hands

Calorie Restriction Curbs Proinflammation That Accompanies Arterial Aging, Preserving a Youthful Phenotype

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