ArticleAmerican journal of physiology. Cell physiology2010
Dexamethasone stimulates store-operated calcium entry and protein degradation in cultured L6 myotubes through a phospholipase A(2)-dependent mechanism.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- In vivo effects of dexamethasone on blood gene expression in ataxia telangiectasia.Molecular and cellular biochemistry · 2018Trial
- Dexamethasone-Induced Fatty Acid Oxidation and Autophagy/Mitophagy Are Essential for T-ALL Glucocorticoid Resistance.Cancers · 2023Article
- Biomimetic cardiac tissue culture model (CTCM) to emulate cardiac physiology and pathophysiology ex vivo.Communications biology · 2022Article
- Intermittent glucocorticoid treatment enhances skeletal muscle performance through sexually dimorphic mechanisms.The Journal of clinical investigation · 2022Article
- Cortisol modulates calcium release-activated calcium channel gating in fish hepatocytes.Scientific reports · 2021Article
- Mechanisms and Clinical Applications of Glucocorticoid Steroids in Muscular Dystrophy.Journal of neuromuscular diseases · 2021Review
- Long-term dexamethasone treatment diminishes store-operated CaInternational journal of oral science · 2019Article
- Glucocorticoid stimulation increases cardiac contractility by SGK1-dependent SOCE-activation in rat cardiac myocytes.PloS one · 2019Article
- Article
- Effects of cyclopiazonic acid and dexamethasone on serotonin-induced calcium responses in vascular smooth muscle cells.Journal of physiology and biochemistry · 2016Article
- Loss of muscle strength during sepsis is in part regulated by glucocorticoids and is associated with reduced muscle fiber stiffness.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Article
- Severe disturbance in the Ca2+ signaling in astrocytes from mouse models of human infantile neuroaxonal dystrophy with mutated Pla2g6.Human molecular genetics · 2012Article
- Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Corticosteroids and muscle wasting: role of transcription factors, nuclear cofactors, and hyperacetylation.Current opinion in clinical nutrition and metabolic care · 2010Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Muscle wasting in various catabolic conditions is at least in part regulated by glucocorticoids. Increased calcium levels have been reported in atrophying muscle. Mechanisms regulating calcium homeostasis in muscle wasting, in particular the role of glucocorticoids, are poorly understood. Here we tested the hypothesis that glucocorticoids increase intracellular calcium concentrations in skeletal muscle and stimulate store-operated calcium entry (SOCE) and that these effects of glucocorticoids may at least in part be responsible for glucocorticoid-induced protein degradation. Treatment of cultured myotubes with dexamethasone, a frequently used in vitro model of muscle wasting, resulted in increased intracellular calcium concentrations determined by fura-2 AM fluorescence measurements. When SOCE was measured by using calcium "add-back" to muscle cells after depletion of intracellular calcium stores, results showed that SOCE was increased 15-25% by dexamethasone and that this response to dexamethasone was inhibited by the store-operated calcium channel blocker BTP2. Dexamethasone treatment stimulated the activity of calcium-independent phospholipase A(2) (iPLA(2)), and dexamethasone-induced increase in SOCE was reduced by the iPLA(2) inhibitor bromoenol lactone (BEL). In additional experiments, treatment of myotubes with the store-operated calcium channel inhibitor gadolinium ion or BEL reduced dexamethasone-induced increase in protein degradation. Taken together, the results suggest that glucocorticoids increase calcium concentrations in myocytes and stimulate iPLA(2)-dependent SOCE and that glucocorticoid-induced muscle protein degradation may at least in part be regulated by increased iPLA(2) activity, SOCE, and cellular calcium levels.
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