ArticleJournal of muscle research and cell motility2015
Dyad content is reduced in cardiac myocytes of mice with impaired calmodulin regulation of RyR2.
Article in Journal of muscle research and cell motility, 2015. 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, 22 citations in OpenAlex.
- Phosphorylation of RyR2 simultaneously expands the dyad and rearranges the tetramers.The Journal of general physiology · 2024Article
- Intracellular to Interorgan Mitochondrial Communication in Striated Muscle in Health and Disease.Endocrine reviews · 2023Review
- Feedback contributions to excitation-contraction coupling in native functioning striated muscle.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Electron microscopy of cardiac 3D nanodynamics: form, function, future.Nature reviews. Cardiology · 2022Review
- The Builders of the Junction: Roles of Junctophilin1 and Junctophilin2 in the Assembly of the Sarcoplasmic Reticulum-Plasma Membrane Junctions in Striated Muscle.Biomolecules · 2022Review
- Structural and Functional Characterization of a NaCirculation research · 2021Article
- Interaction of the Joining Region in Junctophilin-2 With the L-Type CaCirculation research · 2021Article
- Article
- Elongated mitochondrial constrictions and fission in muscle fatigue.Journal of cell science · 2018Article
- Cardiac Arrhythmias as Manifestations of Nanopathies: An Emerging View.Frontiers in physiology · 2018Review
- Neuronal sodium channels: emerging components of the nano-machinery of cardiac calcium cycling.The Journal of physiology · 2017Review
- Cardiovascular consequences of metabolic syndrome.Translational research : the journal of laboratory and clinical medicine · 2017Review
- Increased mitochondrial nanotunneling activity, induced by calcium imbalance, affects intermitochondrial matrix exchanges.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Cardiac T-Tubule Microanatomy and Function.Physiological reviews · 2017Review
- BIN1 regulates dynamic t-tubule membrane.Biochimica et biophysica acta · 2016Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
In cardiac muscle, calmodulin (CaM) regulates the activity of several membrane proteins involved in Ca(2+) homeostasis (CaV1.2; RyR2, SERCA2, PMCA). Three engineered amino acid substitutions in the CaM binding site of the cardiac ryanodine receptor (RyR2) in mice (Ryr2 (ADA/ADA) ) strongly affect cardiac function, with impaired CaM inhibition of RyR2, reduced SR Ca(2+) sequestration, and early cardiac hypertrophy and death (Yamaguchi et al., J Clin Invest 117:1344-1353, 2007). We have examined the ultrastructure and RyR2 immunolocalization in WT and Ryr2 (ADA/ADA) hearts at ~10 days after birth. The myocytes show only minor evidence of structural damage: some increase in intermyofibrillar space, with occasional areas of irregular SR disposition and an increase in frequency of smaller myofibrils, despite an increase of about 15 % in average myocyte cross sectional area. Z line streaming, a sign of myofibrillar stress, is limited and fairly rare. Immunolabeling with an anti-RyR2 antibody shows that RyR-positive foci located at the level of the Z lines are less frequent in mutant hearts. A dramatic decrease in the frequency and size of dyads, accompanied by a decrease in occupancy of the gap by RyR2, but without obvious alterations in location and general structure is a notable ultrastructural feature. The data suggest that the uneven distribution of dyads or calcium release sites within the cells resulting from an overall reduction in RyR2 content may contribute to the poor cardiac performance and early death of Ryr2 (ADA/ADA) mice. An unusual fragmentation of mitochondria, perhaps related to imbalances in free cytoplasmic calcium levels, accompanies these changes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.