ArticlePloS one2013
Abnormal Ca2+ spark/STOC coupling in cerebral artery smooth muscle cells of obese type 2 diabetic mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 39 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Experimental Models for Studying Cardiovascular Dysfunction in Metabolic Syndrome.Handbook of experimental pharmacology · 2026Review
- The SERCA Pump: A Key Molecular Target in Calcium Handling of Vascular Smooth Muscle Cells in Metabolic Syndrome.Handbook of experimental pharmacology · 2026Review
- Aldosterone increases the expression and subcellular localization of SERCA2a and SERCA2b in the rat mesenteric artery.Frontiers in physiology · 2026Article
- Insulin resistance, CaFrontiers in physiology · 2025Review
- Sorbs2 Deficiency and Vascular BK Channelopathy in Diabetes.Circulation research · 2024Article
- SparkMaster 2: A New Software for Automatic Analysis of Calcium Spark Data.Circulation research · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- Vasoprotective Effects of Hyperoside against Cerebral Ischemia/Reperfusion Injury in Rats: Activation of Large-Conductance CaNeural plasticity · 2023Article
- Large-Conductance Calcium-Activated Potassium Channel Opener, NS1619, Protects Against Mesenteric Artery Remodeling Induced by Agonistic Autoantibodies Against the Angiotensin II Type 1 Receptor.Journal of the American Heart Association · 2022Article
- Aldosterone-Induced Sarco/Endoplasmic Reticulum CaFrontiers in physiology · 2022Article
- Heart failure in diabetes.Metabolism: clinical and experimental · 2021Review
- Elementary calcium release events in the skeletal muscle cells of the honey bee Apis mellifera.Scientific reports · 2021Article
- The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.Comprehensive Physiology · 2021Article
- MicroRNA-210 Mediates Hypoxia-Induced Repression of Spontaneous Transient Outward Currents in Sheep Uterine Arteries During Gestation.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle.Cellular and molecular life sciences : CMLS · 2021Review
- Coronary Large Conductance CaFrontiers in physiology · 2021Review
- Aging exacerbates impairments of cerebral blood flow autoregulation and cognition in diabetic rats.GeroScience · 2020Article
- Reduced CaAging · 2020Article
- Disruption of Pressure-Induced CaHypertension (Dallas, Tex. : 1979) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes is a major risk factor for stroke. However, the molecular mechanisms involved in cerebral artery dysfunction found in the diabetic patients are not completely elucidated. In cerebral artery smooth muscle cells (CASMCs), spontaneous and local increases of intracellular Ca2+ due to the opening of ryanodine receptors (Ca2+ sparks) activate large conductance Ca2+-activated K+ (BK) channels that generate spontaneous transient outward currents (STOCs). STOCs have a key participation in the control of vascular myogenic tone and blood pressure. Our goal was to investigate whether alterations in Ca(2+) spark and STOC activities, measured by confocal microscopy and patch-clamp technique, respectively, occur in isolated CASMCs of an experimental model of type-2 diabetes (db/db mouse). We found that mean Ca(2+) spark amplitude, duration, size and rate-of-rise were significantly smaller in Fluo-3 loaded db/db compared to control CASMCs, with a subsequent decrease in the total amount of Ca(2+) released through Ca(2+) sparks in db/db CASMCs, though Ca(2+) spark frequency remained. Interestingly, the frequency of large-amplitude Ca(2+) sparks was also significantly reduced in db/db cells. In addition, the frequency and amplitude of STOCs were markedly reduced at all voltages tested (from -50 to 0 mV) in db/db CASMCs. The latter correlates with decreased BK channel β1/α subunit ratio found in db/db vascular tissues. Taken together, Ca(2+) spark alterations lead to inappropriate BK channels activation in CASMCs of db/db mice and this condition is aggravated by the decrease in the BK β1 subunit/α subunit ratio which underlies the significant reduction of Ca(2+) spark/STOC coupling in CASMCs of diabetic animals.
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