CaMKII activation in early diabetic hearts induces altered sarcoplasmic reticulum-mitochondria signaling

Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca 2+ leak and arrhythmias due to increased activity of the Ca 2+ /calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondr...

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Published inScientific reports Vol. 11; no. 1; pp. 20025 - 16
Main Authors Federico, Marilen, Zavala, Maite, Vico, Tamara, López, Sofía, Portiansky, Enrique, Alvarez, Silvia, Abrille, Maria Celeste Villa, Palomeque, Julieta
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 08.10.2021
Nature Publishing Group
Nature Portfolio
Subjects
631/443
631/443/592
Animals
Arrhythmias, Cardiac - physiopathology
Ca2+/calmodulin-dependent protein kinase II
Calcium (intracellular)
Calcium (mitochondrial)
Calcium (reticular)
Calcium - metabolism
Calcium Signaling - physiology
Calcium-binding protein
Calcium-Binding Proteins - metabolism
Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism
Calmodulin
Cardiomyocytes
Diabetes mellitus
Diabetes Mellitus - physiopathology
Diet
Fusion protein
Heart
Humanities and Social Sciences
Hydrogen peroxide
Hyperactivity
Kinases
Leak channels
Mice
Mice, Transgenic
Mitochondria
Mitochondria - metabolism
Mitochondria - ultrastructure
multidisciplinary
Myocardium
Myocardium - metabolism
Myocardium - pathology
Myocardium - ultrastructure
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - ultrastructure
Oxygen - metabolism
Oxygen consumption
Proteins
Respiration
Retention capacity
Ryanodine
Ryanodine Receptor Calcium Release Channel - metabolism
Ryanodine receptors
Sarcoplasmic reticulum
Sarcoplasmic Reticulum - metabolism
Sarcoplasmic Reticulum - ultrastructure
Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism
Science
Science (multidisciplinary)
Transgenic mice
Transmission electron microscopy
Online AccessGet full text

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Abstract Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca 2+ leak and arrhythmias due to increased activity of the Ca 2+ /calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca 2+ , and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca 2+ release events in FRD vs. CD WT cardiomyocytes. [ 3 H]-Ryanodine binding assay revealed higher [ 3 H]Ry binding in FRD than CD WT hearts. O 2 consumption at State 4 and hydrogen peroxide (H 2 O 2 ) production rate were increased, while respiratory control rate (RCR) and Ca 2+ retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca 2+ leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca 2+ leak by RyR2 activation which in turn increases mitochondria Ca 2+ content due to the enhanced SR-mitochondria tethering, decreasing CRC.
AbstractList Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca 2+ leak and arrhythmias due to increased activity of the Ca 2+ /calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca 2+ , and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca 2+ release events in FRD vs. CD WT cardiomyocytes. [ 3 H]-Ryanodine binding assay revealed higher [ 3 H]Ry binding in FRD than CD WT hearts. O 2 consumption at State 4 and hydrogen peroxide (H 2 O 2 ) production rate were increased, while respiratory control rate (RCR) and Ca 2+ retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca 2+ leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca 2+ leak by RyR2 activation which in turn increases mitochondria Ca 2+ content due to the enhanced SR-mitochondria tethering, decreasing CRC.
Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca2+ leak and arrhythmias due to increased activity of the Ca2+/calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca2+, and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca2+ release events in FRD vs. CD WT cardiomyocytes. [3H]-Ryanodine binding assay revealed higher [3H]Ry binding in FRD than CD WT hearts. O2 consumption at State 4 and hydrogen peroxide (H2O2) production rate were increased, while respiratory control rate (RCR) and Ca2+ retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca2+ leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca2+ leak by RyR2 activation which in turn increases mitochondria Ca2+ content due to the enhanced SR-mitochondria tethering, decreasing CRC.
Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca2+ leak and arrhythmias due to increased activity of the Ca2+/calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca2+, and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca2+ release events in FRD vs. CD WT cardiomyocytes. [3H]-Ryanodine binding assay revealed higher [3H]Ry binding in FRD than CD WT hearts. O2 consumption at State 4 and hydrogen peroxide (H2O2) production rate were increased, while respiratory control rate (RCR) and Ca2+ retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca2+ leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca2+ leak by RyR2 activation which in turn increases mitochondria Ca2+ content due to the enhanced SR-mitochondria tethering, decreasing CRC.Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca2+ leak and arrhythmias due to increased activity of the Ca2+/calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca2+, and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca2+ release events in FRD vs. CD WT cardiomyocytes. [3H]-Ryanodine binding assay revealed higher [3H]Ry binding in FRD than CD WT hearts. O2 consumption at State 4 and hydrogen peroxide (H2O2) production rate were increased, while respiratory control rate (RCR) and Ca2+ retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca2+ leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca2+ leak by RyR2 activation which in turn increases mitochondria Ca2+ content due to the enhanced SR-mitochondria tethering, decreasing CRC.
Abstract Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca2+ leak and arrhythmias due to increased activity of the Ca2+/calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca2+, and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca2+ release events in FRD vs. CD WT cardiomyocytes. [3H]-Ryanodine binding assay revealed higher [3H]Ry binding in FRD than CD WT hearts. O2 consumption at State 4 and hydrogen peroxide (H2O2) production rate were increased, while respiratory control rate (RCR) and Ca2+ retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca2+ leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca2+ leak by RyR2 activation which in turn increases mitochondria Ca2+ content due to the enhanced SR-mitochondria tethering, decreasing CRC.
Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca leak and arrhythmias due to increased activity of the Ca /calmodulin protein kinase II (CaMKII). However, little is known about the role of SR-mitochondria microdomains, mitochondrial structure, and mitochondrial metabolisms. To address this knowledge gap we measured SR-mitochondrial proximity, intracellular Ca , and mitochondrial metabolism in wild type (WT) and AC3-I transgenic mice, with myocardial-targeted CaMKII inhibition, fed with control diet (CD) or with FRD. Confocal images showed significantly increased spontaneous Ca release events in FRD vs. CD WT cardiomyocytes. [ H]-Ryanodine binding assay revealed higher [ H]Ry binding in FRD than CD WT hearts. O consumption at State 4 and hydrogen peroxide (H O ) production rate were increased, while respiratory control rate (RCR) and Ca retention capacity (CRC) were decreased in FRD vs. CD WT isolated mitochondria. Transmission Electron Microscopy (TEM) images showed increased proximity at the SR-mitochondria microdomains, associated with increased tethering proteins, Mfn2, Grp75, and VDAC in FRD vs. CD WT. Mitochondria diameter was decrease and roundness and density were increased in FRD vs. CD WT specimens. The fission protein, Drp1 was significantly increased while the fusion protein, Opa1 was unchanged in FRD vs. CD WT hearts. These differences were prevented in AC3-I mice. We conclude that SR-mitochondria microdomains are subject to CaMKII-dependent remodeling, involving SR-Ca leak and mitochondria fission, in prediabetic mice induced by FRD. We speculate that CaMKII hyperactivity induces SR-Ca leak by RyR2 activation which in turn increases mitochondria Ca content due to the enhanced SR-mitochondria tethering, decreasing CRC.
ArticleNumber 20025
Author Federico, Marilen
Vico, Tamara
López, Sofía
Palomeque, Julieta
Zavala, Maite
Alvarez, Silvia
Portiansky, Enrique
Abrille, Maria Celeste Villa
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34625584$$D View this record in MEDLINE/PubMed
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SSID ssj0000529419
Score 2.4181237
Snippet Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca 2+ leak and arrhythmias due to increased...
Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca leak and arrhythmias due to increased...
Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca2+ leak and arrhythmias due to increased...
Abstract Prediabetic myocardium, induced by fructose-rich diet (FRD), is prone to increased sarcoplasmic reticulum (SR)-Ca2+ leak and arrhythmias due to...
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pubmedcentral
proquest
pubmed
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SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 20025
SubjectTerms 631/443
631/443/592
Animals
Arrhythmias, Cardiac - physiopathology
Ca2+/calmodulin-dependent protein kinase II
Calcium (intracellular)
Calcium (mitochondrial)
Calcium (reticular)
Calcium - metabolism
Calcium Signaling - physiology
Calcium-binding protein
Calcium-Binding Proteins - metabolism
Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism
Calmodulin
Cardiomyocytes
Diabetes mellitus
Diabetes Mellitus - physiopathology
Diet
Fusion protein
Heart
Humanities and Social Sciences
Hydrogen peroxide
Hyperactivity
Kinases
Leak channels
Mice
Mice, Transgenic
Mitochondria
Mitochondria - metabolism
Mitochondria - ultrastructure
multidisciplinary
Myocardium
Myocardium - metabolism
Myocardium - pathology
Myocardium - ultrastructure
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - ultrastructure
Oxygen - metabolism
Oxygen consumption
Proteins
Respiration
Retention capacity
Ryanodine
Ryanodine Receptor Calcium Release Channel - metabolism
Ryanodine receptors
Sarcoplasmic reticulum
Sarcoplasmic Reticulum - metabolism
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Title CaMKII activation in early diabetic hearts induces altered sarcoplasmic reticulum-mitochondria signaling
URI https://link.springer.com/article/10.1038/s41598-021-99118-x
https://www.ncbi.nlm.nih.gov/pubmed/34625584
https://www.proquest.com/docview/2580183737
https://www.proquest.com/docview/2580700552
https://pubmed.ncbi.nlm.nih.gov/PMC8501049
https://doaj.org/article/8a54e36dee0342b9aa851469f3efb5b0
Volume 11
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