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Title:
Depressing Mitochondria-Reticulum Interactions Protects Cardiomyocytes From Lethal Hypoxia-Reoxygenation Injury
Description:
Supporting: 12, Contrasting: 1, Mentioning: 206 - M itochondria and the endoplasmic reticulum (ER) are separately considered key players in cell death signaling.1 Mitochondria and ER are interconnected organelles and form an endomembrane network. The contact points through which ER communicates with mitochondria are referred to as mitochondria-associated membranes (MAM).2 MAM are enriched in phospholipid-and glycosphingolipid-synthesis enzymes, as well as chaperone proteins, which transport lipids and exchange calcium between these 2 organelles.1 Several recent studies have identified new proteins enriched at the ER-mitochondria interface, highlighting the emerging understanding of the role of this region within the cell.3,4 One of them has identified a macromolecular complex composed of VDAC1, Grp75, and IP3R1 that regulates direct Ca 2+ transfer from ER to mitochondria. 5 Indeed, ER-mitochondria junctions are aligned with mitochondrial contact points where VDAC1 is abundantly present, thus creating a hot spot for the Ca 2+ transfer from the ER. 6 Although the role of this organelle cross talk is beginning to be understood in cell physiology, MAM involvement in cardiac pathologies remains unknown. Clinical Perspective on p 1565Calcium signaling is central for heart function through its physiological role in excitation-contraction coupling and the detrimental impact of Ca 2+ overload during heart failure and myocardial ischemia/reperfusion. During this latter condition, it is well accepted that the cytosolic accumulation of Ca 2+ subsequently results in mitochondrial Ca 2+ overload,Background-Under physiological conditions, Ca 2+ transfer from the endoplasmic reticulum (ER) to mitochondria might occur at least in part at contact points between the 2 organelles and involves the VDAC1/Grp75/IP3R1 complex. Accumulation of Ca 2+ into the mitochondrial matrix may activate the mitochondrial chaperone cyclophilin D (CypD) and trigger permeability transition pore opening, whose role in ischemia/reperfusion injury is well recognized. We questioned here whether the transfer of Ca 2+ from ER to mitochondria might play a role in cardiomyocyte death after hypoxia-reoxygenation. Methods and Results-We report that CypD interacts with the VDAC1/Grp75/IP3R1 complex in cardiomyocytes. Genetic or pharmacological inhibition of CypD in both H9c2 cardiomyoblasts and adult cardiomyocytes decreased the Ca 2+ transfer from ER to mitochondria through IP3R under normoxic conditions. During hypoxia-reoxygenation, the interaction between CypD and the IP3R1 Ca 2+ channeling complex increased concomitantly with mitochondrial Ca 2+ content. Inhibition of either CypD, IP3R1, or Grp75 decreased protein interaction within the complex, attenuated mitochondrial Ca 2+ overload, and protected cells from hypoxia-reoxygenation. Genetic or pharmacological inhibition of CypD provided a similar effect in adult mice cardiomyocytes. Disruption of ER-mitochondria interaction via the downregulation of Mfn2 similarly reduced the interaction between CypD and the IP3R1 complex and protected against hypoxia-reo...
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sad, anticipation, social, activity, studies, anxiety, neural, stimuli, examined, speech, task, abstract, mitochondria, show, gskβ, transfer, mams, mentioning, control, confidence, exaggerated, anticipatory, common, disorder, neuroimaging, revealed, altered, response, fewer, feared, current, study, time, magnitude, threat, processing, brain, regions, socially, anxious, individuals, healthy, controls, method, participants, underwent, functional, magnetic, resonance, imaging,
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advanced search capabilities sr/er-mitochondria calcium crosstalk scholarly content—building ethical blog terms results mentioning confidence introduction mentioning confidence smart citation index lethal hypoxia-reoxygenation injury ai-powered research tool google privacy policy 220 citation statements vdac-grp75-ip3r complex depressing er-mitochondria interactions smart citation discussion mentioning confidence show abstract berberine al mentioning confidence copyright-compliant research scite assistant social anxiety disorder transparent ai tools research solutions family reperfusion injury gomez1 show abstract “…pharmacological examined neural activity set email alerts pierre‐alain thiébaut3 cell death signaling glycosphingolipid-synthesis enzymes lab-tech slides current study examined socially anxious individuals 30 mm tris-hcl feared social stimuli mitochondria links alterations er-mitochondria interactions er membrane integrity calcium transfer show abstract “…19 ca 2+ transfer information overload service apply �” mentioning confidence contact points research solutions evaluate scientific literature dashboard cited 2015diabetologiaself cite 14121080 endoplasmic reticulum exchange calcium
Schema {🗺️}
PublicationIssue:
id:#issue
issueNumber:14
datePublished:2013
isPartOf:
id:#periodical
type:
PublicationVolume
Periodical
name:Circulation
issn:
0009-7322
1524-4539
volumeNumber:128
publisher:Ovid Technologies (Wolters Kluwer Health)
["PublicationVolume","Periodical"]:
id:#periodical
name:Circulation
issn:
0009-7322
1524-4539
volumeNumber:128
publisher:Ovid Technologies (Wolters Kluwer Health)
ScholarlyArticle:
isPartOf:#issue
description:M itochondria and the endoplasmic reticulum (ER) are separately considered key players in cell death signaling.1 Mitochondria and ER are interconnected organelles and form an endomembrane network. The contact points through which ER communicates with mitochondria are referred to as mitochondria-associated membranes (MAM).2 MAM are enriched in phospholipid-and glycosphingolipid-synthesis enzymes, as well as chaperone proteins, which transport lipids and exchange calcium between these 2 organelles.1 Several recent studies have identified new proteins enriched at the ER-mitochondria interface, highlighting the emerging understanding of the role of this region within the cell.3,4 One of them has identified a macromolecular complex composed of VDAC1, Grp75, and IP3R1 that regulates direct Ca 2+ transfer from ER to mitochondria. 5 Indeed, ER-mitochondria junctions are aligned with mitochondrial contact points where VDAC1 is abundantly present, thus creating a hot spot for the Ca 2+ transfer from the ER. 6 Although the role of this organelle cross talk is beginning to be understood in cell physiology, MAM involvement in cardiac pathologies remains unknown.
Clinical Perspective on p 1565Calcium signaling is central for heart function through its physiological role in excitation-contraction coupling and the detrimental impact of Ca 2+ overload during heart failure and myocardial ischemia/reperfusion. During this latter condition, it is well accepted that the cytosolic accumulation of Ca 2+ subsequently results in mitochondrial Ca 2+ overload,Background-Under physiological conditions, Ca 2+ transfer from the endoplasmic reticulum (ER) to mitochondria might occur at least in part at contact points between the 2 organelles and involves the VDAC1/Grp75/IP3R1 complex. Accumulation of Ca 2+ into the mitochondrial matrix may activate the mitochondrial chaperone cyclophilin D (CypD) and trigger permeability transition pore opening, whose role in ischemia/reperfusion injury is well recognized. We questioned here whether the transfer of Ca 2+ from ER to mitochondria might play a role in cardiomyocyte death after hypoxia-reoxygenation. Methods and Results-We report that CypD interacts with the VDAC1/Grp75/IP3R1 complex in cardiomyocytes. Genetic or pharmacological inhibition of CypD in both H9c2 cardiomyoblasts and adult cardiomyocytes decreased the Ca 2+ transfer from ER to mitochondria through IP3R under normoxic conditions. During hypoxia-reoxygenation, the interaction between CypD and the IP3R1 Ca 2+ channeling complex increased concomitantly with mitochondrial Ca 2+ content. Inhibition of either CypD, IP3R1, or Grp75 decreased protein interaction within the complex, attenuated mitochondrial Ca 2+ overload, and protected cells from hypoxia-reoxygenation. Genetic or pharmacological inhibition of CypD provided a similar effect in adult mice cardiomyocytes. Disruption of ER-mitochondria interaction via the downregulation of Mfn2 similarly reduced the interaction between CypD and the IP3R1 complex and protected against hypoxia-reo...
abstract:M itochondria and the endoplasmic reticulum (ER) are separately considered key players in cell death signaling.1 Mitochondria and ER are interconnected organelles and form an endomembrane network. The contact points through which ER communicates with mitochondria are referred to as mitochondria-associated membranes (MAM).2 MAM are enriched in phospholipid-and glycosphingolipid-synthesis enzymes, as well as chaperone proteins, which transport lipids and exchange calcium between these 2 organelles.1 Several recent studies have identified new proteins enriched at the ER-mitochondria interface, highlighting the emerging understanding of the role of this region within the cell.3,4 One of them has identified a macromolecular complex composed of VDAC1, Grp75, and IP3R1 that regulates direct Ca 2+ transfer from ER to mitochondria. 5 Indeed, ER-mitochondria junctions are aligned with mitochondrial contact points where VDAC1 is abundantly present, thus creating a hot spot for the Ca 2+ transfer from the ER. 6 Although the role of this organelle cross talk is beginning to be understood in cell physiology, MAM involvement in cardiac pathologies remains unknown.
Clinical Perspective on p 1565Calcium signaling is central for heart function through its physiological role in excitation-contraction coupling and the detrimental impact of Ca 2+ overload during heart failure and myocardial ischemia/reperfusion. During this latter condition, it is well accepted that the cytosolic accumulation of Ca 2+ subsequently results in mitochondrial Ca 2+ overload,Background-Under physiological conditions, Ca 2+ transfer from the endoplasmic reticulum (ER) to mitochondria might occur at least in part at contact points between the 2 organelles and involves the VDAC1/Grp75/IP3R1 complex. Accumulation of Ca 2+ into the mitochondrial matrix may activate the mitochondrial chaperone cyclophilin D (CypD) and trigger permeability transition pore opening, whose role in ischemia/reperfusion injury is well recognized. We questioned here whether the transfer of Ca 2+ from ER to mitochondria might play a role in cardiomyocyte death after hypoxia-reoxygenation. Methods and Results-We report that CypD interacts with the VDAC1/Grp75/IP3R1 complex in cardiomyocytes. Genetic or pharmacological inhibition of CypD in both H9c2 cardiomyoblasts and adult cardiomyocytes decreased the Ca 2+ transfer from ER to mitochondria through IP3R under normoxic conditions. During hypoxia-reoxygenation, the interaction between CypD and the IP3R1 Ca 2+ channeling complex increased concomitantly with mitochondrial Ca 2+ content. Inhibition of either CypD, IP3R1, or Grp75 decreased protein interaction within the complex, attenuated mitochondrial Ca 2+ overload, and protected cells from hypoxia-reoxygenation. Genetic or pharmacological inhibition of CypD provided a similar effect in adult mice cardiomyocytes. Disruption of ER-mitochondria interaction via the downregulation of Mfn2 similarly reduced the interaction between CypD and the IP3R1 complex and protected against hypoxia-reo...
sameAs:https://doi.org/10.1161/circulationaha.113.001225
pagination:1555-1565
name:Depressing Mitochondria-Reticulum Interactions Protects Cardiomyocytes From Lethal Hypoxia-Reoxygenation Injury
headline:Depressing Mitochondria-Reticulum Interactions Protects Cardiomyocytes From Lethal Hypoxia-Reoxygenation Injury
author:
M. Paillard
Emily Tubbs
PierreâAlain Thiébaut
Ludovic Gomez
Jérémy Fauconnier
Claire Crola Da Silva
Geoffrey Teixeira
Nathan Mewton
Elise Belaïdi
Annie Durand
Maryline Abrial
Alain Lacampagne
Jennifer Rieusset
Michel Ovize
publisher:
type:Organization
name:Ovid Technologies (Wolters Kluwer Health)
datePublished:2013
Organization:
name:Ovid Technologies (Wolters Kluwer Health)
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