6 results match your criteria: "Cardiac Signaling Center of MUSC[Affiliation]"
Corrigendum to "Loss-of-function W4645R mutation in the RyR2-caffeine binding site: implications for synchrony and arrhythmogenesis" [Cell Calcium 123 (2024) 102925].
Cell Calcium
December 2024
Cardiac Signaling Center of MUSC, USC and Clemson University, Charleston, SC, USA; Department of Regenerative Medicine and Cell Biology, MUSC, Charleston, SC, USA. Electronic address:
Loss-of-function W4645R mutation in the RyR2-caffeine binding site: implications for synchrony and arrhythmogenesis.
Cell Calcium
November 2024
Cardiac Signaling Center of MUSC, USC and Clemson University, Charleston, SC, USA; Department of Regenerative Medicine and Cell Biology, MUSC,Charleston, SC, USA. Electronic address:
Article Synopsis
- * In experiments with induced pluripotent stem cell-derived cardiomyocytes, this mutation showed no significant change in ionic currents but caused reduced calcium-induced calcium release (CICR) and altered calcium transient relaxation.
- * The mutation led to a complete loss of caffeine-triggered calcium release, increased calcium leakage, and caused arrhythmias, ultimately impairing cardiac function.
Oxygen sensor of the heart.
Can J Physiol Pharmacol
September 2022
Cardiac Signaling Center of MUSC, USC and Clemson, Charleston, SC 29425, USA.
Article Synopsis
- Oxygen sensing in the heart is not well understood, but recent studies indicate that cardiomyocytes can detect low oxygen levels quickly, within seconds.
- Researchers are investigating how acute low oxygen (hypoxia) affects cardiac calcium channels, particularly looking at surface proteins that are involved in this sensing process.
- Key amino acids and phosphorylation sites on the calcium channel’s α-subunit are thought to play crucial roles in oxygen detection, and future experiments with genetically modified models will help clarify these mechanisms.
Mutation in RyR2-FKBP Binding site alters Ca signaling modestly but increases "arrhythmogenesis" in human stem cells derived cardiomyocytes.
Cell Calcium
January 2022
Cardiac Signaling Center of MUSC, USC and Clemson, Charleston, SC, 29425 United States of America; Department of Pharmacology, Georgetown University Medical Center, Washington, DC, United States of America. Electronic address:
Aims: To gain insights into FKBP regulation of cardiac ryanodine receptor (RyR2) and Ca signaling, we introduced the point mutation (N771D-RyR2) corresponding to skeletal muscle mutation (N760D-RyR1) associated with central core disease (CCD) via CRISPR/Cas9 gene-editing in the RyR2 FKBP binding site expressed in human induced pluripotent stem cell-derived cardiomyocytes (hiPSCCMs). Patients inflicted with CCD and other hereditary skeletal muscle diseases often show higher incidence of atrial or ventricular arrhythmias.
Methods And Results: Ca imaging of voltage-clamped N771D-RyR2 mutant compared to WT hiPSCCMs showed: (1) ∼30% suppressed I with no significant changes in the gating kinetics of I; (2) 29% lower SR Ca content and 33% lower RyR2 Ca leak; (3) higher CICR gain and 30-35% increased efficiency of I-triggered Carelease; (4) higher incidence of aberrant SR Ca releases, DADs, and Ca sparks; (5) no change in fractional Ca-release, action potential morphology, sensitivity to isoproterenol, and sarcomeric FKBP-binding pattern.
Regulation of Ca signaling by acute hypoxia and acidosis in cardiomyocytes derived from human induced pluripotent stem cells.
Cell Calcium
March 2019
Cardiac Signaling Center of MUSC, USC and Clemson, Charleston, SC, USA; Department of Pharmacology, Georgetown University Medical Center, Washington, DC, USA. Electronic address:
Aims: The effects of acute (100 s) hypoxia and/or acidosis on Ca signaling parameters of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM) are explored here for the first time.
Methods And Results: 1) hiPSC-CMs express two cell populations: rapidly-inactivating I myocytes (τ<40 ms, in 4-5 day cultures) and slowly-inactivating I (τ ≥ 40 ms, in 6-8 day cultures). 2) Hypoxia suppressed I by 10-20% in rapidly- and 40-55% in slowly-inactivating I cells.
Regulation of Ca signaling by acute hypoxia and acidosis in rat neonatal cardiomyocytes.
J Mol Cell Cardiol
January 2018
Cardiac Signaling Center of MUSC, USC and Clemson, Charleston, SC, USA; Department of Pharmacology, Georgetown University Medical Center, Washington, DC, USA. Electronic address:
Unlabelled: Ischemic heart disease is an arrhythmogenic condition, accompanied by hypoxia, acidosis, and impaired Ca signaling. Here we report on effects of acute hypoxia and acidification in rat neonatal cardiomyocytes cultures.
Results: Two populations of neonatal cardiomyocyte were identified based on inactivation kinetics of L-type I: rapidly-inactivating I (τ~20ms) myocytes (prevalent in 3-4-day cultures), and slow-inactivating I (τ≥40ms) myocytes (dominant in 7-day cultures).