Decrease in regucalcin level and enhancement of protein tyrosine phosphatase activity in rat brain microsomes with increasing age

Tobisawa, Minako; Tsurusaki, Yoshinori; Yamaguchi, Masayoshi

doi:10.3892/ijmm.12.4.577

Cited by 4 publications

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“…A reduced expression of regucalcin could imply an impaired ratio between pro-oxidant and anti-oxidant molecules. It is known that regucalcin levels signiWcantly decrease in aged rats, thus favouring the age-dependent deterioration of liver (Tobisawa et al 2003;Fujita 1999). It seems therefore that senescence pathways are signiWcantly activated in GM-fed mice.…”

Section: Discussionmentioning

confidence: 97%

A long-term study on female mice fed on a genetically modified soybean: effects on liver ageing

Malatesta

Boraldi

Annovi

et al. 2008

Histochem Cell Biol

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Liver represents a suitable model for monitoring the effects of a diet, due to its key role in controlling the whole metabolism. Although no direct evidence has been reported so far that genetically modified (GM) food may affect health, previous studies on hepatocytes from young female mice fed on GM soybean demonstrated nuclear modifications involving transcription and splicing pathways. In this study, the effects of this diet were studied on liver of old female mice in order to elucidate possible interference with ageing. The morpho-functional characteristics of the liver of 24-month-old mice, fed from weaning on control or GM soybean, were investigated by combining a proteomic approach with ultrastructural, morphometrical and immunoelectron microscopical analyses. Several proteins belonging to hepatocyte metabolism, stress response, calcium signalling and mitochondria were differentially expressed in GM-fed mice, indicating a more marked expression of senescence markers in comparison to controls. Moreover, hepatocytes of GM-fed mice showed mitochondrial and nuclear modifications indicative of reduced metabolic rate. This study demonstrates that GM soybean intake can influence some liver features during ageing and, although the mechanisms remain unknown, underlines the importance to investigate the long-term consequences of GM-diets and the potential synergistic effects with ageing, xenobiotics and/or stress conditions.

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Section: Discussionmentioning

confidence: 97%

A long-term study on female mice fed on a genetically modified soybean: effects on liver ageing

Malatesta

Boraldi

Annovi

et al. 2008

Histochem Cell Biol

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“…Brain microsomal protein tyrosine phosphatase activity is increased with increasing age [27]. This enzyme activity is found to be increased in the presence of anti-regucalcin monoclonal antibody in the enzyme reaction mixture, indicating that endogenous regucalcin in brain microsomes may have a suppressive effect on the enzyme activity [27]. The decrease in regucalcin in brain microsomes with aging is partly related to the enhancement of microsomal protein tyrosine phosphatase activity in the brain of aged rats.…”

Section: +mentioning

confidence: 85%

“…Regucalcin is localized in the microsomes of rat brain, and aging causes a decrease in the microsomal regucalcin levels [27]. Brain microsomal protein tyrosine phosphatase activity is increased with increasing age [27]. This enzyme activity is found to be increased in the presence of anti-regucalcin monoclonal antibody in the enzyme reaction mixture, indicating that endogenous regucalcin in brain microsomes may have a suppressive effect on the enzyme activity [27].…”

Section: +mentioning

confidence: 95%

“…Calbindin and S-100A proteins, which are Ca 2+ -binding protein in brain [11], have no effect on protein phosphatase activity in rat brain cytoplasm [26]. Regucalcin is localized in the microsomes of rat brain, and aging causes a decrease in the microsomal regucalcin levels [27]. Brain microsomal protein tyrosine phosphatase activity is increased with increasing age [27].…”

Section: +mentioning

confidence: 99%

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Calcium Regulatory Protein, Regucalcin, may be a Key Molecule in Brain Disease

Yamaguchi¹

2013

J Mol Genet Med

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“…Regucalcin is localized in the microsomes of the rat brain, and aging causes a decrease in the microsomal regucalcin levels. 119 Protein phosphatase 2A has been detected in the brain microsomes of rats. 125 We found that protein tyrosine phosphatase activity is detected in rat brain microsomes.…”

Section: Regucalcin Suppresses Brain Protein Phosphatase Activitymentioning

confidence: 99%

Role of regucalcin in brain calcium signaling: involvement in aging

Yamaguchi

2012

Integrative Biology

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Regucalcin was discovered in 1978 to be a calcium-binding protein that does not contain the EF-hand motif of the calcium-binding domain [M. Yamaguchi and T. Yamamoto, Chem. Pharm. Bull., 26, 1915-1918, 1978]. The regucalcin gene is localized on the X chromosome and its expression is enhanced through various transcription factors. Regucalcin is known to play a multifunctional role as a suppressor protein of cell signaling in many cell types. Regucalcin is expressed in rat brain neurons and it is decreased in the cerebral cortex and hippocampus of the brain with aging. Neuronal Ca(2+) signaling has been implicated in mechanisms of neuronal plasticity like long-term potentiation, which is likely to play an important role in learning and memory. The disturbance of brain Ca(2+) homeostasis may play a pivotal role in the revelation of brain disease. The intracellular Ca(2+) in brain tissues is increased with aging. Aging enhances the entry of Ca(2+) into brain neuronal cells across the plasma membranes. An increase in the brain microsomal Ca(2+)-ATPase activity of rats with aging resulted in calcium accumulation in the microsomes of the Ca(2+)-sequestrating system that is partly related to the brain toxicity by calcium. Regucalcin had an inhibitory effect on rat brain microsomal Ca(2+)-ATPase activity. The suppressive effect of regucalcin on brain microsomal Ca(2+)-ATPase activity was weakened in aged rats. Regucalcin was found to inhibit brain cytosolic protein kinase C. Brain microsomal Ca(2+)-ATPase activity was enhanced by protein kinase C in aged rats. Regucalcin could also inhibit activity of Ca(2+)/calmodulin-dependent protein kinase, protein phosphatase, and Ca(2+)/calmodulin-dependent nitric oxide synthase, which is linked to Ca(2+) signaling, in the cytosol of rat brain neurons. These inhibitory effects of regucalcin were weakened with aging. Regucalcin may play a pivotal role in the regulation of Ca(2+) signaling which is stimulated through a neurotransmitter in the brain neurons with aging.

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Decrease in regucalcin level and enhancement of protein tyrosine phosphatase activity in rat brain microsomes with increasing age

Cited by 4 publications

References 0 publications

A long-term study on female mice fed on a genetically modified soybean: effects on liver ageing

A long-term study on female mice fed on a genetically modified soybean: effects on liver ageing

Calcium Regulatory Protein, Regucalcin, may be a Key Molecule in Brain Disease

Role of regucalcin in brain calcium signaling: involvement in aging

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