ArticleCardiovascular research2011
T-type Ca²+ signalling regulates aldosterone-induced CREB activation and cell death through PP2A activation in neonatal cardiomyocytes.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Calcium-Dependent Regulation of Neuronal Excitability Is Rescued in Fragile X Syndrome by a Tat-Conjugated N-Terminal Fragment of FMRP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- New Perspectives on Sex Steroid and Mineralocorticoid Receptor Signaling in Cardiac Ischemic Injury.Frontiers in physiology · 2022Review
- Association between CaExperimental gerontology · 2021Article
- Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression.International journal of molecular sciences · 2021Article
- Berberine: A Review of its Pharmacokinetics Properties and Therapeutic Potentials in Diverse Vascular Diseases.Frontiers in pharmacology · 2021Review
- Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?International journal of molecular sciences · 2018Review
- MicroRNA-204 Is Necessary for Aldosterone-Stimulated T-Type Calcium Channel Expression in Cardiomyocytes.International journal of molecular sciences · 2018Article
- RhoA inhibits the hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes via positively regulating the CREB phosphorylation.Bioscience reports · 2017Article
- CREB1 directly activates the transcription of ribonucleotide reductase small subunit M2 and promotes the aggressiveness of human colorectal cancer.Oncotarget · 2016Article
- Fragile X mental retardation protein controls ion channel expression and activity.The Journal of physiology · 2016Review
- Transient Receptor Potential Canonical (TRPC)/Orai1-dependent Store-operated Ca2+ Channels: NEW TARGETS OF ALDOSTERONE IN CARDIOMYOCYTES.The Journal of biological chemistry · 2016Article
- Aldosterone down-regulates the slowly activated delayed rectifier potassium current in adult guinea pig cardiomyocytes.British journal of pharmacology · 2015Article
- T-type Calcium Channel Regulation of Neural Tube Closure and EphrinA/EPHA Expression.Cell reports · 2015Article
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- Protein Phosphatase 2A Mediates Oxidative Stress Induced Apoptosis in Osteoblasts.Mediators of inflammation · 2015Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsWe have investigated Ca²(+) signalling generated by aldosterone-induced T-type current (I(CaT)), the effects of I(CaT) in neonatal cardiomyocytes, and a putative role for I(CaT) in cardiomyocytes during cardiac pathology induced by stenosis in an adult rat. METHODS AND
resultsNeonatal rat cardiomyocytes treated with aldosterone showed an increase in I(CaT) density, principally due to the upregulation of the T-type channel Ca(v)3.1 (by 80%). Aldosterone activated cAMP-response element-binding protein (CREB), and this activation was enhanced by blocking I(CaT) or by inhibiting protein phosphatase 2A (PP2A) activity. Aldosterone induced PP2A activity, an induction that was prevented upon I(CaT) blockade. I(CaT) exerted a negative feedback regulation on the transcription of the Ca(v)3.1 gene, and the activation of PP2A by I(CaT) led to increased levels of the pro-apoptotic markers caspase 9 and Bcl-x(S) and decreased levels of the anti-apoptotic marker Bcl-2. These findings were corroborated by flow cytometry analysis for apoptosis and necrosis. Similarly, in a rat model of cardiac disease, I(CaT) re-emergence was associated with a decrease in CREB activation and was correlated with increases in caspase 9 and Bcl-x(S) and a decrease in Bcl-2 levels.
conclusionOur findings establish PP2A/CREB as targets of I(CaT)-generated Ca²(+) signalling and identify an important role for I(CaT) in cardiomyocyte cell death.
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Registered trials
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