Adenine Nucleotide Translocator in Heart

Portman, Michael A.

doi:10.1006/mgme.2000.3030

Cited by 13 publications

(6 citation statements)

References 53 publications

(60 reference statements)

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“…The exchange through the adenine nucleotide translocator (ANT) occurs in coordination with proton reflux through the mitochondrial ATP synthase (Harris and Das, 1991). In fact, the ANT is reported to be the most prominent single protein component of the inner mitochondrial membrane (Portman, 2000). The role of ANT in the regulation of mitochondrial respiration may be exaggerated if the amount of this protein is limited in either quantity or activity.…”

Section: Discussionmentioning

confidence: 99%

Depletion of adenine nucleotide translocator protein in heart mitochondria from doxorubicin-treated rats—Relevance for mitochondrial dysfunction

Oliveira

Wallace

2006

Toxicology

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Section: Discussionmentioning

confidence: 99%

Depletion of adenine nucleotide translocator protein in heart mitochondria from doxorubicin-treated rats—Relevance for mitochondrial dysfunction

Oliveira

Wallace

2006

Toxicology

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“…In the liver, where, with the possible exception of Cyp. D [39], the candidate proteins for the putative MPTP organization are present as tissue‐specific isoforms with respect to the heart [40,41], lower concentrations of Ca 2+ would suffice to assemble the classical CsA sensitive MPTP. It has also to be taken into consideration the very different content of ANT protein in mitochondria from liver and heart.…”

Section: Discussionmentioning

confidence: 99%

Arachidonic acid induces specific membrane permeability increase in heart mitochondria

Paola¹,

Oliveros-Celis²,

Lorusso³

2006

FEBS Letters

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Micromolar concentrations of arachidonic acid cause in Ca 2+ loaded heart mitochondria matrix swelling and Ca 2+ release. These effects appear to be unrelated to the classical membrane permeability transition (MPT), as they are CsA insensitive, membrane potential independent and can also be activated by Sr 2+ . Atractyloside potentiated and ATP inhibited the arachidonic acid induced swelling. These observations suggest that the ATP/ADP translocator (ANT) may be involved in the AA induced, CsA insensitive membrane permeability increase. Under the same experimental conditions used for heart mitochondria, arachidonic acid induced the classical CsA sensitive, ADP inhibitable MPT in liver mitochondria.

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“…ANT‐1 mutant mice exhibited severe cardiomyopathy (38). Impaired ANT‐1 function and increased ANT‐1 levels were observed in heart tissue from patients with dilated cardiomyopathy (51), and point mutations in the ANT‐1 gene have been reported in humans to generate genetic mitochondrial disease (52). ANT‐1 overexpression leads to the phenotypic alteration of the apoptosis, i.e., collapsed mitochondrial membrane potential, cytochrome c release, caspase activation, and DNA degradation (53).…”

Section: Discussionmentioning

confidence: 99%

Serotonin is a novel survival factor of cardiomyocytes: mitochondria as a target of 5‐HT_2B‐receptor signaling

et al. 2003

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Identification of factors regulating cardiomyocyte survival and growth is important to understand the pathogenesis of congenital heart diseases. Little is known about the molecular mechanism of cardiac functions triggered by serotonin. The link between signaling circuitry of external stimuli and the mitochondrial apoptotic machinery is of wide interest in cardiac diseases. Using cultured cardiomyocytes and 5-hydroxytryptamine (5-HT)2B-receptor knockout mice as an animal model of dilated cardiomyopathy, for the first time we show that serotonin via the Gq-coupled 5-HT2B-receptor protect cardiomyocytes against serum deprivation-induced apoptosis as manifested by DNA fragmentation, nuclear chromatin condensation, and TUNEL labeling. Serotonin prevents cytochrome c release and caspase-9 and -3 activation after serum deprivation via cross-talks between phosphatidylinositol-3 kinase/Akt and extracellular signal-regulated kinase (ERK) 1/2 signaling pathways. Serotonin binding to 5-HT2B-receptor activates ERK kinases to inhibit Bax expression induced by serum deprivation. Serotonin via phosphatidylinositol-3 kinase/Akt can activate NF-kappaB that is required for the regulation of the mitochondrial adenine nucleotide translocator (ANT-1). Parallel to these observations, ultrastructural analysis in the 5-HT2B-receptor knockout mice heart revealed pronounced mitochondrial defects in addition to altered mitochondrial enzyme activities (cytochrome oxidase and succinate dehydrogenase) and ANT-1 and Bax expressions. These findings identify 5-HT as a novel survival factor targeting mitochondria in cardiomyocytes.

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Adenine Nucleotide Translocator in Heart

Cited by 13 publications

References 53 publications

Depletion of adenine nucleotide translocator protein in heart mitochondria from doxorubicin-treated rats—Relevance for mitochondrial dysfunction

Depletion of adenine nucleotide translocator protein in heart mitochondria from doxorubicin-treated rats—Relevance for mitochondrial dysfunction

Arachidonic acid induces specific membrane permeability increase in heart mitochondria

Serotonin is a novel survival factor of cardiomyocytes: mitochondria as a target of 5‐HT_2B‐receptor signaling

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Adenine Nucleotide Translocator in Heart

Cited by 13 publications

References 53 publications

Depletion of adenine nucleotide translocator protein in heart mitochondria from doxorubicin-treated rats—Relevance for mitochondrial dysfunction

Depletion of adenine nucleotide translocator protein in heart mitochondria from doxorubicin-treated rats—Relevance for mitochondrial dysfunction

Arachidonic acid induces specific membrane permeability increase in heart mitochondria

Serotonin is a novel survival factor of cardiomyocytes: mitochondria as a target of 5‐HT2B‐receptor signaling

Contact Info

Product

Resources

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Serotonin is a novel survival factor of cardiomyocytes: mitochondria as a target of 5‐HT_2B‐receptor signaling