Protein oxidation and age-dependent alterations in calcium homeostasis

Squier, Thomas C.

doi:10.2741/a530

Cited by 103 publications

(68 citation statements)

References 80 publications

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“…Most physiological and histological studies of fibre aging indicate that sarcopenia is due to a multi-factorial pathology. Skeletal muscle aging is associated with a wide variety of cellular, biochemical and physiological alterations, including (i) grouped atrophying fibres, increased numbers of centrally located nuclei and variability in fibre diameter [9], (ii) metabolic alterations [43], (iii) mitochondrial disturbances and an increased susceptibility to apoptosis [44], (iv) a decreased regenerative capacity [45], (v) disturbed luminal ion binding and cycling [46], (vi) excitation-contraction uncoupling [47], (vii) oxidative stress [48], (viii) a blunted cellular stress response [49], (ix) impaired protein synthesis of myofibrillar components [50], ( (x) denervation-associated atrophy [51], (xi) an altered equilibrium of growth factors and hormones involved in fibre maintenance [52], and (xii) a severe decline in contractile efficiency [53]. Our proteomic map of alterations in protein expression in the aqueous versus detergent-extracted fractions from aged muscle agrees with the idea of complex biochemical changes in sarcopenia.…”

Section: Discussionmentioning

confidence: 99%

DIGE analysis of rat skeletal muscle proteins using nonionic detergent phase extraction of young adult versus aged gastrocnemius tissue

Donoghue

Staunton

Mullen

et al. 2010

Journal of Proteomics

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Contractile weakness and loss of muscle mass are critical features of the aging process in mammalians. Age-related fibre wasting has a profound effect on muscle metabolism, fibre type distribution and the overall physiological integrity of the neuromuscular system. This study has used mass spectrometry-based proteomics to investigate the fate of the aging rat muscle proteome. Using nonionic detergent phase extraction, this report shows that the aged gastrocnemius muscle exhibits a generally perturbed protein expression pattern in both the detergent-extracted fraction and the aqueous protein complement from senescent muscle tissue. In the detergent-extracted fraction, the expression of ATP synthase, isocitrate dehydrogenase, enolase, tropomyosin and beta-actin was increased. Different isoforms of creatine kinase and prohibitin showed differential changes. In the aqueous fraction, malate dehydrogenase, sulfotransferase, triosephosphate isomerase, aldolase, cofilin-2 and lactate dehydrogenase showed increased levels. Interestingly, differential effects on dissimilar 2-D spots of the same protein species were shown for Cu/Zn superoxide dismutase, albumin, annexin A4 and phosphoglycolate phosphatase. Mitochondrial Hsp60, Hsp71 and nucleoside diphosphate kinase B exhibited a reduced abundance in aged muscle. The majority of altered proteins were found to be involved in mitochondrial metabolism, glycolysis, metabolic transportation, regulatory processes, the cellular stress response, detoxification mechanisms and muscle contraction.

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Section: Discussionmentioning

confidence: 99%

DIGE analysis of rat skeletal muscle proteins using nonionic detergent phase extraction of young adult versus aged gastrocnemius tissue

Donoghue

Staunton

Mullen

et al. 2010

Journal of Proteomics

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“…Indeed, better comprehension of the features that distinguish a normal, "healthy" old brain from a brain that is at an early stage of a neurodegenerative disease is a key aspect in developing treatments. This is important because inflammatory and oxidative responses do promote alterations in calcium signaling (for review see Squier and Bigelow, 2000), which is the pri- mary signaling mechanism by which astrocytes modulate neuronal function and could thus be critical for the progression from the "aged" to the "diseased" brain.…”

Section: Astrocytes In the Aging Brainmentioning

confidence: 99%

“…IL-1 can differentially regulate calcium wave propagation by switching between a gap junction-mediated event to a purinergic-mediated pathway (John et al, 1999). Oxidation in the calcium signaling protein calmodulin (CaM) alters the maintenance of intracellular calcium levels and changes the transport activity of the plasma membrane Ca-ATPase of aged muscle and neuronal cells (Squier and Bigelow, 2000). Oxidation of the thiol groups in the IP 3 receptor will lower the threshold IP 3 concentration for calcium release (Peuchen et al, 1996), promoting amplified calcium responses (Fig.…”

Section: Do Aged Astrocytes Altermentioning

confidence: 99%

Astrocytes in the aging brain

Cotrina¹,

Nedergaard²

2002

J. Neurosci. Res.

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“…Cells are exposed to oxidative stress as a result of one or more of three factors: i) increase in oxidant generation, ii) decrease in antioxidant protection, and iii) failure to repair oxidative damage. ROS cause damage to lipids, nucleic acids and proteins (Berlett and Stadtman, 1997;Mecocci et al, 1999), and lead to a functional deficit in the control of Ca 2+ homeostasis in myofibers as a consequence (Eu et al, 2000;Fulle et al, 2004;Fulle et al 2005;Squier and Bigelow, 2000).…”

Section: Introductionmentioning

confidence: 99%

Molecular basis of the myogenic profile of aged human skeletal muscle satellite cells during differentiation

Pietrangelo¹,

Puglielli²,

Mancinelli³

et al. 2009

Experimental Gerontology

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ular basis of the myogenic profile of aged human skeletal muscle satellite cells during differentiation. Experimental Gerontology, Elsevier, 2009, 44 (8) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 2 ACCEPTED MANUSCRIPT ACCEPTED MANUSCRIPT AbstractSarcopenia is the age-related loss of muscle mass, strength and function. Human muscle proteins are synthesized at a slower rate in the elderly than in young adults, leading to atrophy and muscle mass loss with a decline in the functional capability. Additionally, aging is accompanied by a decrease in the ability of muscle tissue to regenerate following injury or overuse due to the impairment of intervening satellite cells, in which we previously reported oxidative damage evidences. The aim of the present study was to determine the effects of aging on myoblasts and myotubes obtained from human skeletal muscle, and characterize the transcriptional profile as molecular expression patterns in relation to age-dependent modifications in their regenerative capacity. Our data show that the failure to differentiate does not depend on reduced myogenic cell number, but difficulty to complete the differentiation program. Data reported here suggested the following findings: i) oxidative damage accumulation in molecular substrates, probably due to impaired antioxidant activity and insufficient repair capability, ii) limited capability of elderly myoblasts to execute a complete differentiation program; restricted fusion, possibly due to altered cytoskeleton turnover and extracellular matrix degradation, and iii) activation of atrophy mechanism by activation of a specific FOXO-dependent program.

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Protein oxidation and age-dependent alterations in calcium homeostasis

Cited by 103 publications

References 80 publications

DIGE analysis of rat skeletal muscle proteins using nonionic detergent phase extraction of young adult versus aged gastrocnemius tissue

DIGE analysis of rat skeletal muscle proteins using nonionic detergent phase extraction of young adult versus aged gastrocnemius tissue

Astrocytes in the aging brain

Molecular basis of the myogenic profile of aged human skeletal muscle satellite cells during differentiation

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