Energy‐Linked Ion Movements in Mitochondrial Systems

Lehninger, Albert L.; Carafoli, Ernesto; Rossi, C

doi:10.1002/9780470122747.ch6

Cited by 245 publications

(30 citation statements)

References 140 publications

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“…We also used the Ca 2+ uniporter blocker, Ru360 (10 µM, 30 min) to prevent entry of free Ca 2+ into the mitochondrial matrix (Matlib et al, 1998; Wu et al, 2007). Since FCCP and Ru360 can also deplete ATP, we used oligomycin (8 ng/ml, 30 min) as a control to inhibit ATP synthesis; oligomycin does not inhibit mitochondrial Ca 2+ accumulation when substrate oxidation is functional (Lehninger et al, 1967). …”

Section: Resultsmentioning

confidence: 99%

Mitochondria Modulate Ca²⁺-Dependent Glutamate Release from Rat Cortical Astrocytes

Reyes¹,

Parpura²

2008

J. Neurosci.

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Section: Resultsmentioning

confidence: 99%

Mitochondria Modulate Ca²⁺-Dependent Glutamate Release from Rat Cortical Astrocytes

Reyes¹,

Parpura²

2008

J. Neurosci.

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“…Contrary to previous reports showing that siRNA-mediated partial depletion of PiC in cultured cells had no effect on MPTP opening, 27 we discovered that the complete loss of PiC protein in AdCre-treated Slc25a3 fl/fl primary MEFs resulted in a delayed dissipation of mitochondrial calcein signal in response to Ca In addition to the requirement of Pi for ATP synthesis, Pi is known to serve as an accompanying anion for mitochondrial Ca 2 þ uptake. 29,30 Thus, one possibility for the Slc25a3 deletion-mediated desensitization of the MPTP is that mitochondrial Ca 2 þ uptake could be impaired. However, we observed that the protective effect of Slc25a3 deletion was not due to impaired mitochondrial Ca 2 þ uptake, as mitochondria from these gene-targeted mice exhibited an enhanced uptake ability.…”

Section: Discussionmentioning

confidence: 99%

Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy

et al. 2014

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The mitochondrial phosphate carrier (PiC) is critical for ATP synthesis by serving as the primary means for mitochondrial phosphate import across the inner membrane. In addition to its role in energy production, PiC is hypothesized to have a role in cell death as either a component or a regulator of the mitochondrial permeability transition pore (MPTP) complex. Here, we have generated a mouse model with inducible and cardiac-specific deletion of the Slc25a3 gene (PiC protein). Loss of PiC protein did not prevent MPTP opening, suggesting it is not a direct pore-forming component of this complex. However, Slc25a3 deletion in the heart blunted MPTP opening in response to Ca 2 þ challenge and led to a greater Ca 2 þ uptake capacity. This desensitization of MPTP opening due to loss or reduction in PiC protein attenuated cardiac ischemic-reperfusion injury, as well as partially protected cells in culture from Ca 2 þ overload induced death. Intriguingly, deletion of the Slc25a3 gene from the heart long-term resulted in profound hypertrophy with ventricular dilation and depressed cardiac function, all features that reflect the cardiomyopathy observed in humans with mutations in SLC25A3. Together, these results demonstrate that although the PiC is not a direct component of the MPTP, it can regulate its activity, suggesting a novel therapeutic target for reducing necrotic cell death. In addition, mice lacking Slc25a3 in the heart serve as a novel model of metabolic, mitochondrial-driven cardiomyopathy. The mitochondrial oxidative phosphorylation (OXPHOS) system is the primary source of cellular energy production. Defects in OXPHOS occur with a frequency of 1 in 5000 live births 1 and underlie a wide range of mitochondrial disorders that often affect multiple organ systems and tissues with high oxidative energy demands, such as brain, skeletal muscle, and heart.2 Cardiac phenotypes associated with mitochondrial disease are diverse, and can range from cardiomyopathies to cardiac conduction defects. [3][4][5]

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“…This ability of mitochondria provides them with an opportunity to take part in the processes of biologic calcination and decalcination, i.e. the general regulation of metabolism inside the cell [59,60].…”

Section: The Heritage Of Mineral Crystalmentioning

confidence: 99%

The Possibility of the Formation of Protocells and Their Structural Components on the Basis of the Apatite Matrix and Cocrystallizing Minerals

Kostetsky

2005

J Biol Phys

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Abstract. This paper presents the author's theory on the possibility of simultaneous hard-phase synthesis of various organic molecules from gas-phase elements on the basis of the apatite matrix and cocrystallizing minerals (carbonate-apatite, calcite, mica). These molecules and their ensembles gave rise to living systems and protocells of the pro-and eukaryotic types. Synthesis might have occurred through gradual substitution of the mineral matrix by crystal organic matter. The structure and size of the molecules synthesized were determined by the structure, physical parameters, and arrangement of organizing centers in the crystal lattice. Apatite phosphates were embedded in a synthesized nucleic helix and their size and purine-pyrimidine complementarity were determined. Apatite and cocrystallizing minerals were seen to be involved in the synthesis of four basic classes of cell components: apatite-DNA and nucleoproteide complexes; carbonate-apatite-enzymes, other proteins involved in DNA replication, all RNA types and their complexes with the specific proteins and enzymes of transcription and translation; calcite-cytoskeletal proteins; and mica-membrane lipids and proteins. The evidence supporting this theory is presented. A possible mechanism to account for the transition from crystal through organo-mineral crystal to liquid crystal (protocell) and a model of the occurrence of the matrix mechanism of transcription and translation are proposed. Some principal problems in the biochemistry and molecular biology of the origin of life on the Earth are discussed.Key words: origin of life, protocells, minerals, organo-mineral crystal, liquid crystal, molecular evolution, matrix mechanism Abbreviations: NA, nucleic acid; NP, nucleoprotein; EC, elementary cell; Ap-DNA, apatite DNA (hypothetical model based on the apatite crystal structure)

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Energy‐Linked Ion Movements in Mitochondrial Systems

Cited by 245 publications

References 140 publications

Mitochondria Modulate Ca²⁺-Dependent Glutamate Release from Rat Cortical Astrocytes

Mitochondria Modulate Ca²⁺-Dependent Glutamate Release from Rat Cortical Astrocytes

Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy

The Possibility of the Formation of Protocells and Their Structural Components on the Basis of the Apatite Matrix and Cocrystallizing Minerals

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Energy‐Linked Ion Movements in Mitochondrial Systems

Cited by 245 publications

References 140 publications

Mitochondria Modulate Ca2+-Dependent Glutamate Release from Rat Cortical Astrocytes

Mitochondria Modulate Ca2+-Dependent Glutamate Release from Rat Cortical Astrocytes

Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy

The Possibility of the Formation of Protocells and Their Structural Components on the Basis of the Apatite Matrix and Cocrystallizing Minerals

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Mitochondria Modulate Ca²⁺-Dependent Glutamate Release from Rat Cortical Astrocytes

Mitochondria Modulate Ca²⁺-Dependent Glutamate Release from Rat Cortical Astrocytes