Effect of hydrogen peroxide on calcium homeostasis in smooth muscle cells
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Cited by (151)
Understanding the relationship between oxidative stress and cognition in the elderly: Targets for nutraceutical interventions
2020, Nutraceuticals in Brain Health and BeyondMitochondrial calcium uniporter in Drosophila transfers calcium between the endoplasmic reticulum and mitochondria in oxidative stress-induced cell death
2017, Journal of Biological ChemistryCitation Excerpt :Oxidative stress is proposed as the main causative factor for neurodegenerative, cardiovascular, and other mitochondria-related diseases (46). Previous studies reported that oxidative stress increases [Ca2+]i (47–49), although there are controversies whether the source of Ca2+ is from the extracellular environment or intracellular stores. We observed marked and sustained [Ca2+]mito rises by exogenous oxidative stress inducers, such as H2O2 and t-BuOOH in Drosophila, which have not been investigated previously.
Specific combinations of ion channel inhibitors reduce excessive Ca<sup>2+</sup> influx as a consequence of oxidative stress and increase neuronal and glial cell viability in vitro
2016, NeuroscienceCitation Excerpt :Multiple feed forward mechanisms that result in ROS initiate further increases in intracellular Ca2+ levels, contributing to additional cell death (Kristian and Siesjo, 1998). Proposed mechanisms by which H2O2 causes increased intracellular Ca2+ levels include activation of VGCCs (Roveri et al., 1992), nonspecific changes in membrane permeability to Ca2+ (Rojanasakul et al., 1993), changes in the Na+–Ca2+ exchanger (Kaneko et al., 1989), and H2O2 induced Ca2+ release from intracellular stores (Nicotera and Rossi, 1994). Our data indicate that both release of Ca2+ from ryanodine-sensitive intracellular stores and influx of extracellular Ca2+ through P2X7R as well as other Ca2+ channels contribute to the rise in intracellular Ca2+ levels following H2O2 insult.
Angiotensin II as a limiting agent to intracellular calcium signaling in inflammatory states
2013, Journal of Surgical ResearchAngiotensin II inhibits interleukin-6 mRNA expression of LPS-stimulated macrophages through down-regulating calcium signaling
2013, Journal of Surgical ResearchCitation Excerpt :However, both agents did augment the increase of IL-6 mRNA levels of MØ stimulated by LPS. As previously reported, it is still unclear why only the release the internal calcium stores but not the influx of extracellular calcium directly induces the expression of MØ IL-6 mRNA [30]. The release of intracellular calcium stores from the ER has been linked to the phospholipase C system [9].