Relevance of the plasma membrane calcium-ATPase in the homeostasis of calcium in the fetal liver

Delgado–Coello, Blanca; Mas‐Oliva, Jaime

doi:10.1080/15476278.2015.1011918

Cited by 2 publications

(1 citation statement)

References 50 publications

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“…Although reactive oxygen and nitrogen species for years now have been known to play a key role during the development of several important cell functions, nowadays it is clear that calcium also plays an important role in cell death disrupting normal physiological pathways by triggering either necrotic or apoptotic cell death. Since a state of oxidative stress causes a calcium influx into the cytoplasm either from internal stores such as the endoplasmic reticulum and the mitochondria or from the extracellular space, a concentration increase of calcium in the cytoplasm has been linked with many diseases including atherosclerosis 31 – 33 . Our results showing an important correlation between the response macrophages show when treated with high concentrations of LPS and an increase in the concentration of PMCA in the cell nucleus and cleavage activation of procaspase-7 in the cell cytoplasm, indicate that the state of oxidative stress achieved in our macrophage model is probably also associated to a calcium unbalance.…”

Section: Discussionmentioning

confidence: 99%

A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

Mas‐Oliva

2017

Sci Rep

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Our study tested the proposal that c-Myc activation in macrophages is differentially carried out dependent on the intracellular oxidative state of cells and potentially associated to the process of atherogenesis. Under our experimental conditions, the generation of reactive oxygen species carried out by the presence of oxidized low density lipoproteins (oxLDL) or Gram negative bacterial lipopolysaccharides (LPS) modifies the expression of cellular adhesion molecules such as c-Abl, calcium transport proteins such as the plasma membrane Ca2+-ATPase (PMCA), CD47, procaspase-7, CASP7, CHOP, transcriptional activators such as c-Jun and c-Myc and molecules that participate in the process of endocytosis like α- and β-adaptin. We present the first evidence showing that a state of oxidative stress alters c-Myc-dependent activity pathways in macrophages through binding to molecules such as β-adaptin promoting the reversible formation of a complex that presents the ability to regulate the development of the cell cycle. We propose that the subtle regulation carried out through the formation of this c-Myc/β-adaptin complex when cells change from a normal physiological condition to a state of oxidative stress, represents a defense mechanism against the deleterious effects caused by the loss of cell homeostasis.

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Section: Discussionmentioning

confidence: 99%

A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

Mas‐Oliva

2017

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Protective effects of Alpha-lipoic acid on MeHg-induced oxidative damage and intracellular Ca²⁺dyshomeostasis in primary cultured neurons

Yang

Liu

et al. 2016

Free Radical Research

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Methylmercury (MeHg) is one of the ubiquitous environmental toxicant that leads to long-lasting neurological deficits in animals and humans. However, the mechanisms of MeHg-induced neuronal cell death are incompletely understood. Treatment of neuronal cells with MeHg (0-2 μM) for 0.5-12 h, or pretreated with LA (12.5-100 μM) for 0.5-6 h resulted in toxic effects of primary cultured neurons concentration- and time-dependently. For further experiments, 12.5, 25, and 50 μM of LA pretreatment for 3 h followed by 1 μM MeHg for 6 h were performed for the examination of the responses of neurons. Exposure of MeHg resulted in damages of neurons, which were shown by a loss of cell viability, and supported by high levels of lactate dehydrogenase (LDH) release, apoptosis, and morphological changes. In addition, neurons were sensitive to MeHg-mediated oxidative stress, a finding that is consistent with ROS over-production, leading to decrease Ca(2+)-ATPase activity and increase intracellular free calcium. Moreover, expressions of NMDA receptor subunits in neurons were down-regulated after MeHg exposure, and expression of NR2A mRNA and protein were much more sensitive to MeHg than those of NR1 and NR2B. On the contrary, pretreatment with LA presented a concentration-dependent prevention against MeHg-mediated cytotoxic effects of neurons. In conclusion, present results showed that oxidative stress and intracellular Ca(2+ )dyshomeostasis resulting from MeHg exposure contributed to neuronal injury. LA could attenuate MeHg-induced neuronal toxicity via its antioxidant properties in primary cultured neurons.

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Relevance of the plasma membrane calcium-ATPase in the homeostasis of calcium in the fetal liver

Cited by 2 publications

References 50 publications

A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

Protective effects of Alpha-lipoic acid on MeHg-induced oxidative damage and intracellular Ca²⁺dyshomeostasis in primary cultured neurons

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Relevance of the plasma membrane calcium-ATPase in the homeostasis of calcium in the fetal liver

Cited by 2 publications

References 50 publications

A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

A Novel β-adaptin/c-Myc Complex Formation Modulated by Oxidative Stress in the Control of the Cell Cycle in Macrophages and its Implication in Atherogenesis

Protective effects of Alpha-lipoic acid on MeHg-induced oxidative damage and intracellular Ca2+dyshomeostasis in primary cultured neurons

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Protective effects of Alpha-lipoic acid on MeHg-induced oxidative damage and intracellular Ca²⁺dyshomeostasis in primary cultured neurons