Lack of cystic fibrosis transmembrane regulator -type chloride current in pediatric human atrial myocytes

Berul, Charles I.; Sweeten, Tammy L.; Vetter, Victoria L.; Morad, Martin

doi:10.1016/s0024-3205(96)00615-7

Cited by 12 publications

(4 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since the first electrophysiological recording of CFTR in the heart (Nagel et al 1992), there has been little dispute regarding it being responsible for the cardiac PKA-stimulated Cl − channel. While there have been conflicting reports about CFTR expression and/or activity in humans Berul et al 1997;Du et al 2000), studies have shown that CFTR is expressed, and electrophysiological recordings have been made from rats (Uramoto et al 2003), guinea-pigs (Hume et al 1994), rabbits , swine (Gao et al 2007), dogs (Hume et al 1994), primates and, most pertinent to our study, mice (Lader et al 2000). Despite these studies, questions remain regarding the role of CFTR in the heart.…”

Section: Discussionmentioning

confidence: 99%

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca²⁺‐activated Cl⁻ channel activity to maintain contraction rate

Sellers

Arcangelis²,

Xiang³

et al. 2010

The Journal of Physiology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca²⁺‐activated Cl⁻ channel activity to maintain contraction rate

Sellers

Arcangelis²,

Xiang³

et al. 2010

The Journal of Physiology

View full text Add to dashboard Cite

“…These findings have important implications for those studying cardiac Cl − channels as potential targets for novel antiarrythmic agents. It remains to be determined whether I AB is present in human ventricular muscle, although preliminary evidence suggests that a background Cl − current may be present in human atria (Berul et al ., 1997). Thus, I AB may represent a novel therapeutic target for anti‐arrhythmic agents.…”

Section: Discussionmentioning

confidence: 99%

A novel anionic conductance affects action potential duration in isolated rat ventricular myocytes

Spencer

Uchida

Kozlowski

2000

British J Pharmacology

View full text Add to dashboard Cite

Eects of extracellular anions were studied in electrophysiological experiments on freshly isolated rat ventricular myocytes. Under current-clamp, action potential duration (APD) -and cyclic AMPindependent, and was unaected by cell shrinkage. I AB was insensitive to stilbene and fenamate anion transport blockers at concentrations that inhibit Ca 2+ -, cyclic AMP-and swelling-activated Cl 7 currents in ventricular cells of other mammals. These results suggest that I AB may be carried by a novel class of Cl 7 channel. Correlation of anion substitution experiments on membrane current and action potentials revealed that I AB could play a major role in controlling rat ventricular APD. These ®ndings have important implications for those studying cardiac Cl 7 channels as potential targets for novel antiarrythmic agents.

show abstract

“…Other complicating factors in studies of human myocardial tissue are alterations as a result of disease, drugs, or age of patients and practical difficulties usually associated with obtaining viable human myocardial samples in a timely fashion for enzymatic dispersion. Human atrial myocytes isolated from pediatric patients (aged 1 day to 11 yr) also failed to exhibit detectable I Cl.PKA , even though many cells appeared to express a basally active Cl Ϫ conductance that was inhibited by 9-AC (25). It seems clear from animal studies that CFTR expression is highest and I Cl.PKA is most consistently detected in ventricular myocytes, compared with atrial myocytes, where only 10 -15% of the cells may express CFTR (cf.…”

Section: Recent Controversiesmentioning

confidence: 98%

Anion Transport in Heart

Hume

Duan

Collier

et al. 2000

Physiological Reviews

205

239

View full text Add to dashboard Cite

Anion transport proteins in mammalian cells participate in a wide variety of cell and intracellular organelle functions, including regulation of electrical activity, pH, volume, and the transport of osmolites and metabolites, and may even play a role in the control of immunological responses, cell migration, cell proliferation, and differentiation. Although significant progress over the past decade has been achieved in understanding electrogenic and electroneutral anion transport proteins in sarcolemmal and intracellular membranes, information on the molecular nature and physiological significance of many of these proteins, especially in the heart, is incomplete. Functional and molecular studies presently suggest that four primary types of sarcolemmal anion channels are expressed in cardiac cells: channels regulated by protein kinase A (PKA), protein kinase C, and purinergic receptors (I(Cl.PKA)); channels regulated by changes in cell volume (I(Cl.vol)); channels activated by intracellular Ca(2+) (I(Cl.Ca)); and inwardly rectifying anion channels (I(Cl.ir)). In most animal species, I(Cl.PKA) is due to expression of a cardiac isoform of the epithelial cystic fibrosis transmembrane conductance regulator Cl(-) channel. New molecular candidates responsible for I(Cl.vol), I(Cl.Ca), and I(Cl.ir) (ClC-3, CLCA1, and ClC-2, respectively) have recently been identified and are presently being evaluated. Two isoforms of the band 3 anion exchange protein, originally characterized in erythrocytes, are responsible for Cl(-)/HCO(3)(-) exchange, and at least two members of a large vertebrate family of electroneutral cotransporters (ENCC1 and ENCC3) are responsible for Na(+)-dependent Cl(-) cotransport in heart. A 223-amino acid protein in the outer mitochondrial membrane of most eukaryotic cells comprises a voltage-dependent anion channel. The molecular entities responsible for other types of electroneutral anion exchange or Cl(-) conductances in intracellular membranes of the sarcoplasmic reticulum or nucleus are unknown. Evidence of cardiac expression of up to five additional members of the ClC gene family suggest a rich new variety of molecular candidates that may underlie existing or novel Cl(-) channel subtypes in sarcolemmal and intracellular membranes. The application of modern molecular biological and genetic approaches to the study of anion transport proteins during the next decade holds exciting promise for eventually revealing the actual physiological, pathophysiological, and clinical significance of these unique transport processes in cardiac and other mammalian cells.

show abstract

Lack of cystic fibrosis transmembrane regulator -type chloride current in pediatric human atrial myocytes

Cited by 12 publications

References 24 publications

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca²⁺‐activated Cl⁻ channel activity to maintain contraction rate

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca²⁺‐activated Cl⁻ channel activity to maintain contraction rate

A novel anionic conductance affects action potential duration in isolated rat ventricular myocytes

Anion Transport in Heart

Contact Info

Product

Resources

About

Lack of cystic fibrosis transmembrane regulator -type chloride current in pediatric human atrial myocytes

Cited by 12 publications

References 24 publications

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca2+‐activated Cl− channel activity to maintain contraction rate

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca2+‐activated Cl− channel activity to maintain contraction rate

A novel anionic conductance affects action potential duration in isolated rat ventricular myocytes

Anion Transport in Heart

Contact Info

Product

Resources

About

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca²⁺‐activated Cl⁻ channel activity to maintain contraction rate

Cardiomyocytes with disrupted CFTR function require CaMKII and Ca²⁺‐activated Cl⁻ channel activity to maintain contraction rate