Protein oxidation and age-dependent alterations in calcium homeostasis

Squier, Thomas C.; Bigelow, Diana J.

doi:10.2741/squier

Cited by 153 publications

(97 citation statements)

References 171 publications

(34 reference statements)

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“…Cystein thiol groups are particularly sensitive to oxidation by reactive oxygen or nitrogen species (Squier and Bigelow 2000;Cohen and Adachi 2006;Ying et al 2007Ying et al , 2008. Modification of reactive cysteine thiols resulting in generation of disulfides not only affects protein structure but can alter the function of proteins by modulation of enzymatic activity (Cohen and Adachi 2006).…”

Section: Discussionmentioning

confidence: 99%

Oxidative injury induced by hypochlorous acid to Ca-ATPase from sarcoplasmic reticulum of skeletal muscle and protective effect of trolox

Štrosová

Karlovska²,

Spickett

et al. 2009

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Abstract. Hypochlorous acid (HOCl) concentration-dependently decreased ATPase activity and SH groups of pure Ca-ATPase from sarcoplasmic reticulum (SERCA) of rabbit skeletal muscle with IC 50 of 150 µmol/l and 6.6 µmol/l, respectively. This indicates that SH goups were not critical for impairment of Ca-ATPase activity. Pure Ca-ATPase activity was analysed individually with respect to both substrates, Ca 2+

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Section: Discussionmentioning

confidence: 99%

Oxidative injury induced by hypochlorous acid to Ca-ATPase from sarcoplasmic reticulum of skeletal muscle and protective effect of trolox

Štrosová

Karlovska²,

Spickett

et al. 2009

gpb

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“…The connection between CHOP upregulation and NOX signaling in AD remains to be further clarified but it seems to be a good target for future therapeutic perspectives. Another positive feedback is played by ROS itself that can sensitize both Ca 2+ -release channels and SERCA at the ER membrane [227–229]. ROS or RNS can oxidize critical thiols in the RyR, causing Ca 2+ release [230].…”

Section: Er and Oxidative Stress In Admentioning

confidence: 99%

Mitochondrial- and Endoplasmic Reticulum-Associated Oxidative Stress in Alzheimer's Disease: From Pathogenesis to Biomarkers

Ferreiro

Baldeiras

Ferreira

et al. 2012

International Journal of Cell Biology

130

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Alzheimer's disease (AD) is the most common cause of dementia in the elderly, affecting several million of people worldwide. Pathological changes in the AD brain include the presence of amyloid plaques, neurofibrillary tangles, loss of neurons and synapses, and oxidative damage. These changes strongly associate with mitochondrial dysfunction and stress of the endoplasmic reticulum (ER). Mitochondrial dysfunction is intimately linked to the production of reactive oxygen species (ROS) and mitochondrial-driven apoptosis, which appear to be aggravated in the brain of AD patients. Concomitantly, mitochondria are closely associated with ER, and the deleterious crosstalk between both organelles has been shown to be involved in neuronal degeneration in AD. Stimuli that enhance expression of normal and/or folding-defective proteins activate an adaptive unfolded protein response (UPR) that, if unresolved, can cause apoptotic cell death. ER stress also induces the generation of ROS that, together with mitochondrial ROS and decreased activity of several antioxidant defenses, promotes chronic oxidative stress. In this paper we discuss the critical role of mitochondrial and ER dysfunction in oxidative injury in AD cellular and animal models, as well as in biological fluids from AD patients. Progress in developing peripheral and cerebrospinal fluid biomarkers related to oxidative stress will also be summarized.

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“…An age-related decline in the function of these transports systems has been suggested to underlie altered Ca 2+ homeostasis during brain aging and contribute to age-related neurodegenerative diseases (Michaelis et al, 1984, 1996; Zaidi et al, 1998; Hanahisa and Yamaguchi, 2001; Pottorf et al, 2001; Gomez-Villafuertes et al, 2007). The decrease in activity may be linked to oxidation of pump proteins or CBPs that regulate pump activity (Zaidi and Michaelis, 1999; Squier and Bigelow, 2000; Bartlett et al, 2003). As such, it is likely that altered pump activity will vary with regional differences in oxidative stress.…”

Section: Ca2+ Buffering Extrusion and Sequestrationmentioning

confidence: 99%

Susceptibility to calcium dysregulation during brain aging

Kumar

Bodhinathan

Foster

2009

Front. Ag. Neurosci.

110

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Calcium (Ca2+) is a highly versatile intracellular signaling molecule that is essential for regulating a variety of cellular and physiological processes ranging from fertilization to programmed cell death. Research has provided ample evidence that brain aging is associated with altered Ca2+ homeostasis. Much of the work has focused on the hippocampus, a brain region critically involved in learning and memory, which is particularly susceptible to dysfunction during senescence. The current review takes a broader perspective, assessing age-related changes in Ca2+ sources, Ca2+ sequestration, and Ca2+ binding proteins throughout the nervous system. The nature of altered Ca2+ homeostasis is cell specific and may represent a deficit or a compensatory mechanism, producing complex patterns of impaired cellular function. Incorporating the knowledge of the complexity of age-related alterations in Ca2+ homeostasis will positively shape the development of highly effective therapeutics to treat brain disorders.

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Protein oxidation and age-dependent alterations in calcium homeostasis

Cited by 153 publications

References 171 publications

Oxidative injury induced by hypochlorous acid to Ca-ATPase from sarcoplasmic reticulum of skeletal muscle and protective effect of trolox

Oxidative injury induced by hypochlorous acid to Ca-ATPase from sarcoplasmic reticulum of skeletal muscle and protective effect of trolox

Mitochondrial- and Endoplasmic Reticulum-Associated Oxidative Stress in Alzheimer's Disease: From Pathogenesis to Biomarkers

Susceptibility to calcium dysregulation during brain aging

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