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Article ; Online: MCU-independent Ca

Bround, Michael J / Abay, Eaman / Huo, Jiuzhou / Havens, Julian R / York, Allen J / Bers, Donald M / Molkentin, Jeffery D

Scientific reports

2024 Volume 14, Issue 1, Page(s) 6751

Abstract: Mitochondrial ... ...

Abstract	Mitochondrial Ca
MeSH term(s)	Animals ; Humans ; Mice ; Calcium/metabolism ; Calcium Channels/metabolism ; Cell Death ; Mitochondria/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Muscular Dystrophy, Duchenne/pathology ; Necrosis/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Calcium Channels ; Mitochondrial Membrane Transport Proteins ; Mcu protein, mouse
Language	English
Publishing date	2024-03-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-57340-3
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Article ; Online: Increasing SERCA function promotes initiation of calcium sparks and breakup of calcium waves.

Sato, Daisuke / Uchinoumi, Hitoshi / Bers, Donald M

The Journal of physiology

2021 Volume 599, Issue 13, Page(s) 3267–3278

Abstract: Key points: Increasing sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA) pump activity enhances sarcoplasmic reticulum calcium (Ca) load, which increases both ryanodine receptor opening and driving force of Ca release flux. Both of these effects ...

Abstract	Key points: Increasing sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA) pump activity enhances sarcoplasmic reticulum calcium (Ca) load, which increases both ryanodine receptor opening and driving force of Ca release flux. Both of these effects promote Ca spark formation and wave propagation. However, increasing SERCA activity also accelerates local cytosolic Ca decay as the wave front travels to the next cluster, which limits wave propagation. As a result, increasing SERCA pump activity has a biphasic effect on the propensity of arrhythmogenic Ca waves, but a monotonic effect to increase Ca spark frequency and amplitude. Abstract: Waves of sarcoplasmic reticulum (SR) calcium (Ca) release can cause arrhythmogenic afterdepolarizations in cardiac myocytes. Ca waves propagate when Ca sparks at one Ca release unit (CRU) recruit new Ca sparks in neighbouring CRUs. Under normal conditions, Ca sparks are too small to recruit neighbouring Ca sparks where Ca sensitivity is also low. However, under pathological conditions such as a Ca overload or ryanodine receptor (RyR) sensitization, Ca sparks can be larger and propagate more readily as macro-sparks or full Ca waves. Increasing SERCA pump activity promotes SR Ca load, which promotes RyR opening and increases driving force of the Ca release flux from SR to cytosol, promoting Ca waves. However, high sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA) activity can also decrease local cytosolic [Ca] as it approaches the next CRU, thereby reducing wave appearance and propagation. In this study, we use a physiologically detailed model of subcellular Ca cycling and experiments in phospholamban-knockout mice, to show how Ca waves are initiated and propagate and how different conditions contribute to the generation and propagation of Ca waves. We show that reducing diffusive coupling between Ca sparks by increasing SERCA activity prevents Ca waves by reducing [Ca] at the next CRU, as do Ca buffers, low intra-SR Ca diffusion and distance between CRUs. Increasing SR Ca uptake rate has a biphasic effect on Ca wave propagation; initially it enhances Ca spark probability and amplitude and CRU coupling, thereby promoting arrhythmogenic Ca wave propagation, but at higher levels SR Ca uptake can abort those arrhythmogenic Ca waves.
MeSH term(s)	Animals ; Calcium/metabolism ; Calcium Signaling ; Mice ; Myocytes, Cardiac/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism
Chemical Substances	Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-06-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP281579
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Article: Molecular Mechanism of a FRET Biosensor for the Cardiac Ryanodine Receptor Pathologically Leaky State.

Svensson, Bengt / Nitu, Florentin R / Rebbeck, Robyn T / McGurran, Lindsey M / Oda, Tetsuro / Thomas, David D / Bers, Donald M / Cornea, Razvan L

bioRxiv : the preprint server for biology

2023

Abstract: ... ...

Abstract	Ca
Language	English
Publishing date	2023-07-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.07.548138
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Article ; Online: Molecular Mechanism of a FRET Biosensor for the Cardiac Ryanodine Receptor Pathologically Leaky State.

Svensson, Bengt / Nitu, Florentin R / Rebbeck, Robyn T / McGurran, Lindsey M / Oda, Tetsuro / Thomas, David D / Bers, Donald M / Cornea, Razvan L

International journal of molecular sciences

2023 Volume 24, Issue 16

Abstract: ... ...

Abstract	Ca
MeSH term(s)	Binding Sites ; Drug Delivery Systems ; Fluorescence Resonance Energy Transfer ; Ryanodine Receptor Calcium Release Channel
Chemical Substances	Ryanodine Receptor Calcium Release Channel
Language	English
Publishing date	2023-08-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241612547
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Article ; Online: A 20/20 view of ANT function in mitochondrial biology and necrotic cell death.

Bround, Michael J / Bers, Donald M / Molkentin, Jeffery D

Journal of molecular and cellular cardiology

2020 Volume 144, Page(s) A3–A13

Abstract: The adenosine nucleotide translocase (ANT) family of proteins are inner mitochondrial membrane proteins involved in energy homeostasis and cell death. The primary function of ANT proteins is to exchange cytosolic ADP with matrix ATP, facilitating the ... ...

Abstract	The adenosine nucleotide translocase (ANT) family of proteins are inner mitochondrial membrane proteins involved in energy homeostasis and cell death. The primary function of ANT proteins is to exchange cytosolic ADP with matrix ATP, facilitating the export of newly synthesized ATP to the cell while providing new ADP substrate to the mitochondria. As such, the ANT proteins are central to maintaining energy homeostasis in all eukaryotic cells. Evidence also suggests that the ANTs constitute a pore-forming component of the mitochondrial permeability transition pore (MPTP), a structure that forms in the inner mitochondrial membrane that is thought to underlie regulated necrotic cell death. Additionally, emerging studies suggest that ANT proteins are also critical for mitochondrial uncoupling and for promoting mitophagy. Thus, the ANTs are multifunctional proteins that are poised to participate in several aspects of mitochondrial biology and the greater regulation of cell death, which will be discussed here.
MeSH term(s)	Animals ; Gene Expression Regulation ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial ADP, ATP Translocases/genetics ; Mitochondrial ADP, ATP Translocases/metabolism ; Mitochondrial Membrane Transport Proteins/genetics ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Permeability Transition Pore/metabolism ; Models, Biological ; Multigene Family ; Necroptosis/genetics ; Oxidative Phosphorylation
Chemical Substances	Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; Mitochondrial ADP, ATP Translocases (9068-80-8)
Language	English
Publishing date	2020-05-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2020.05.012
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Article ; Online: Cardiac sarcoplasmic reticulum calcium leak: basis and roles in cardiac dysfunction.

Bers, Donald M

Annual review of physiology

2013 Volume 76, Page(s) 107–127

Abstract: ... diastolic [Ca]i, contributing to diastolic dysfunction; (c) cause triggered arrhythmias; and (d) be ...

Abstract	Synchronized SR calcium (Ca) release is critical to normal cardiac myocyte excitation-contraction coupling, and ideally this release shuts off completely between heartbeats. However, other SR Ca release events are referred to collectively as SR Ca leak (which includes Ca sparks and waves as well as smaller events not detectable as Ca sparks). Much, but not all, of the SR Ca leak occurs via ryanodine receptors and can be exacerbated in pathological states such as heart failure. The extent of SR Ca leak is important because it can (a) reduce SR Ca available for release, causing systolic dysfunction; (b) elevate diastolic [Ca]i, contributing to diastolic dysfunction; (c) cause triggered arrhythmias; and (d) be energetically costly because of extra ATP used to repump Ca. This review addresses quantitative aspects and manifestations of SR Ca leak and its measurement, and how leak is modulated by Ca, associated proteins, and posttranslational modifications in health and disease.
MeSH term(s)	Animals ; Calcium/metabolism ; Calcium Signaling/physiology ; Heart Diseases/metabolism ; Heart Diseases/physiopathology ; Humans ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Rabbits ; Rats ; Ryanodine Receptor Calcium Release Channel/physiology ; Sarcoplasmic Reticulum/metabolism
Chemical Substances	Ryanodine Receptor Calcium Release Channel ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2013-11-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207933-1
ISSN	1545-1585 ; 0066-4278
ISSN (online)	1545-1585
ISSN	0066-4278
DOI	10.1146/annurev-physiol-020911-153308
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Article ; Online: MCUb is an inducible regulator of calcium-dependent mitochondrial metabolism and substrate utilization in muscle.

Huo, Jiuzhou / Prasad, Vikram / Grimes, Kelly M / Vanhoutte, Davy / Blair, N Scott / Lin, Suh-Chin / Bround, Michael J / Bers, Donald M / Molkentin, Jeffery D

Cell reports

2023 Volume 42, Issue 11, Page(s) 113465

Abstract: Mitochondria use the electron transport chain to generate high-energy phosphate from oxidative phosphorylation, a process also regulated by the mitochondrial ... ...

Abstract	Mitochondria use the electron transport chain to generate high-energy phosphate from oxidative phosphorylation, a process also regulated by the mitochondrial Ca
MeSH term(s)	Animals ; Mice ; Calcium/metabolism ; Calcium Channels/metabolism ; Fatty Acids/metabolism ; Mitochondria/metabolism ; Muscle, Skeletal/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Calcium Channels ; Fatty Acids ; Mcub protein, mouse
Language	English
Publishing date	2023-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113465
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Article ; Online: Protein Kinase D1 Regulates Cardiac Hypertrophy, Potassium Channel Remodeling, and Arrhythmias in Heart Failure.

Bossuyt, Julie / Borst, Johanna M / Verberckmoes, Marie / Bailey, Logan R J / Bers, Donald M / Hegyi, Bence

Journal of the American Heart Association

2022 Volume 11, Issue 19, Page(s) e027573

Abstract: Background Structural and electrophysiological remodeling characterize heart failure (HF) enhancing arrhythmias. PKD1 (protein kinase D1) is upregulated in HF and mediates pathological hypertrophic signaling, but its role in K+ channel remodeling and ... ...

Abstract	Background Structural and electrophysiological remodeling characterize heart failure (HF) enhancing arrhythmias. PKD1 (protein kinase D1) is upregulated in HF and mediates pathological hypertrophic signaling, but its role in K+ channel remodeling and arrhythmogenesis in HF is unknown. Methods and Results We performed echocardiography, electrophysiology, and expression analysis in wild-type and PKD1 cardiomyocyte-specific knockout (cKO) mice following transverse aortic constriction (TAC). PKD1-cKO mice exhibited significantly less cardiac hypertrophy post-TAC and were protected from early decline in cardiac contractile function (3 weeks post-TAC) but not the progression to HF at 7 weeks post-TAC. Wild-type mice exhibited ventricular action potential duration prolongation at 8 weeks post-TAC, which was attenuated in PKD1-cKO, consistent with larger K+ currents via the transient outward current, sustained current, inward rectifier K+ current, and rapid delayed rectifier K+ current and increased expression of corresponding K+ channels. Conversely, reduction of slowly inactivating K+ current was independent of PKD1 in HF. Acute PKD inhibition slightly increased transient outward current in TAC and sham wild-type myocytes but did not alter other K+ currents. Sham PKD1-cKO versus wild-type also exhibited larger transient outward current and faster early action potential repolarization. Tachypacing-induced action potential duration alternans in TAC animals was increased and independent of PKD1, but diastolic arrhythmogenic activities were reduced in PKD1-cKO. Conclusions Our data indicate an important role for PKD1 in the HF-related hypertrophic response and K+ channel downregulation. Therefore, PKD1 inhibition may represent a therapeutic strategy to reduce hypertrophy and arrhythmias; however, PKD1 inhibition may not prevent disease progression and reduced contractility in HF.
MeSH term(s)	Animals ; Mice ; Action Potentials/physiology ; Arrhythmias, Cardiac/genetics ; Arrhythmias, Cardiac/metabolism ; Cardiomegaly/metabolism ; Heart Failure/genetics ; Heart Failure/metabolism ; Myocytes, Cardiac/metabolism ; Potassium/metabolism ; Potassium Channels/metabolism ; Protein Kinase C/genetics ; Protein Kinase C/metabolism
Chemical Substances	Potassium (RWP5GA015D) ; Potassium Channels ; Protein Kinase C (EC 2.7.11.13) ; protein kinase D (EC 2.7.10.-)
Language	English
Publishing date	2022-09-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.122.027573
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Article ; Online: Differential sex-dependent susceptibility to diastolic dysfunction and arrhythmia in cardiomyocytes from obese diabetic HFpEF model.

Mira Hernandez, Juliana / Shen, Erin Y / Ko, Christopher Y / Hourani, Zaynab / Spencer, Emily R / Smoliarchuk, Daria / Bossuyt, Julie / Granzier, Henk / Bers, Donald M / Hegyi, Bence

Cardiovascular research

2024

Abstract: Aim: Sex-differences in heart failure with preserved ejection fraction (HFpEF) are important, but key mechanisms involved are incompletely understood. While animal models can inform about sex-dependent cellular and molecular changes, many previous ... ...

Abstract	Aim: Sex-differences in heart failure with preserved ejection fraction (HFpEF) are important, but key mechanisms involved are incompletely understood. While animal models can inform about sex-dependent cellular and molecular changes, many previous preclinical HFpEF models have failed to recapitulate sex-dependent characteristics of human HFpEF. We tested for sex-differences in HFpEF using a two-hit mouse model (leptin receptor-deficient db/db mice plus aldosterone infusion for 4 weeks; db/db+Aldo). Methods and results: We performed echocardiography, electrophysiology, intracellular Ca2+ imaging, and protein analysis. Female HFpEF mice exhibited more severe diastolic dysfunction in line with increased titin N2B isoform expression and PEVK element phosphorylation, and reduced troponin-I phosphorylation. Female HFpEF mice had lower BNP levels than males despite similar comorbidity burden (obesity, diabetes) and cardiac hypertrophy in both sexes. Male HFpEF mice were more susceptible to cardiac alternans. Male HFpEF cardiomyocytes (versus female) exhibited higher diastolic [Ca2+], slower Ca2+ transient decay, reduced L-type Ca2+ current, more pronounced enhancement of the late Na+ current, and increased short-term variability of action potential duration (APD). However, male and female HFpEF myocytes showed similar downregulation of inward rectifier and transient outward K+ currents, APD prolongation, and frequency of delayed afterdepolarizations. Inhibition of Ca2+/calmodulin-dependent protein kinase II (CaMKII) reversed all pathological APD changes in HFpEF in both sexes, and empagliflozin pretreatment mimicked these effects of CaMKII inhibition. Vericiguat had only slight benefits, and these effects were larger in HFpEF females. Conclusion: We conclude that the db/db+Aldo preclinical HFpEF murine model recapitulates key sex-specific mechanisms in HFpEF and provides mechanistic insights into impaired excitation-contraction coupling and sex-dependent differential arrhythmia susceptibility in HFpEF with potential therapeutic implications. In male HFpEF myocytes, altered Ca2+ handling and electrophysiology aligned with diastolic dysfunction and arrhythmias, while worse diastolic dysfunction in females may depend more on altered myofilaments properties.
Language	English
Publishing date	2024-04-26
Publishing country	England
Document type	Journal Article
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvae070
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Article ; Online: CaMKII and PKA-dependent phosphorylation co-regulate nuclear localization of HDAC4 in adult cardiomyocytes.

Helmstadter, Kathryn G / Ljubojevic-Holzer, Senka / Wood, Brent M / Taheri, Khanha D / Sedej, Simon / Erickson, Jeffrey R / Bossuyt, Julie / Bers, Donald M

Basic research in cardiology

2021 Volume 116, Issue 1, Page(s) 11

Abstract: Nuclear histone deacetylase 4 (HDAC4) represses MEF2-mediated transcription, implicated in the development of heart failure. CaMKII-dependent phosphorylation drives nucleus-to-cytoplasm HDAC4 shuttling, but protein kinase A (PKA) is also linked to HDAC4 ... ...

Abstract	Nuclear histone deacetylase 4 (HDAC4) represses MEF2-mediated transcription, implicated in the development of heart failure. CaMKII-dependent phosphorylation drives nucleus-to-cytoplasm HDAC4 shuttling, but protein kinase A (PKA) is also linked to HDAC4 translocation. However, the interplay of CaMKII and PKA in regulating adult cardiomyocyte HDAC4 translocation is unclear. Here we sought to determine the interplay of PKA- and CaMKII-dependent HDAC4 phosphorylation and translocation in adult mouse, rabbit and human ventricular myocytes. Confocal imaging and protein analyses revealed that inhibition of CaMKII-but not PKA, PKC or PKD-raised nucleo-to-cytoplasmic HDAC4 fluorescence ratio (F
MeSH term(s)	Active Transport, Cell Nucleus ; Adrenergic beta-Agonists/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/antagonists & inhibitors ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cardiomegaly/enzymology ; Cardiomegaly/genetics ; Cardiomegaly/pathology ; Cardiomegaly/physiopathology ; Cells, Cultured ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Disease Models, Animal ; Female ; Heart Failure/enzymology ; Heart Failure/genetics ; Heart Failure/pathology ; Heart Failure/physiopathology ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/enzymology ; Myocytes, Cardiac/pathology ; Phosphorylation ; Protein Kinase Inhibitors/pharmacology ; Rabbits ; Repressor Proteins ; Signal Transduction ; Ventricular Remodeling
Chemical Substances	Adrenergic beta-Agonists ; Protein Kinase Inhibitors ; Repressor Proteins ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 (EC 2.7.11.17) ; Camk2g protein, mouse (EC 2.7.11.17) ; HDAC4 protein, human (EC 3.5.1.98) ; Hdac5 protein, mouse (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2021-02-15
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-021-00850-2
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