The Role of Mitochondrial Potassium Fluxes in Controlling the Protonmotive Force in Energized Mitochondria

Czyż, Aneta; Szewczyk, Adam; Nałȩcz, Maciej J.; Wojtczak, Lech

doi:10.1006/bbrc.1995.1632

Cited by 50 publications

(26 citation statements)

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“…Our simulations are compared in Fig. 3D with experimental data by Czyż et al (5). Again, a good agreement can be observed (see also "Discussion").…”

Section: Theoretical Resultssupporting

confidence: 76%

“…This value may change depending on conditions, for instance with the intensity of ATP production by mitochondria. In the great majority of reports, the contribution of ⌬⌿ to ⌬p (u ϭ ⌬⌿/⌬p) of 80 -85% (0.8 -0.85) was reported (2)(3)(4)(5)(6)(7)(8)(9)(10). This means that the value of ⌬pH is around 30 mV (0.5 pH units) (2-10) (again, in older reports, values around 50 mV are sometimes reported (10)).…”

mentioning

confidence: 99%

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Control Over the Contribution of the Mitochondrial Membrane Potential (ΔΨ) and Proton Gradient (ΔpH) to the Protonmotive Force (Δp)

Dzbek

Korzeniewski

2008

Journal of Biological Chemistry

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“…Our simulations are compared in Fig. 3D with experimental data by Czyż et al (5). Again, a good agreement can be observed (see also "Discussion").…”

Section: Theoretical Resultssupporting

confidence: 76%

mentioning

confidence: 99%

Control Over the Contribution of the Mitochondrial Membrane Potential (ΔΨ) and Proton Gradient (ΔpH) to the Protonmotive Force (Δp)

Dzbek

Korzeniewski

2008

Journal of Biological Chemistry

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“…This is in agreement with observations reported by Czyz et al [5] showing that an increase in the cytosolic K + concentration depolarized DeltaPsi. This is also consistent with other reports showing that K + channel openers also depolarized DeltaPsi via a direct action at the level of mitochondrial K + channels [5,7]. Since the intracellular K + concentration was found to affect DeltaPsi, we tested the effect of blocking K + membrane conductances with TEA.…”

Section: Discussionsupporting

confidence: 83%

Mitochondrial Membrane Potential (DeltaPsi) and Ca<sup>2+</sup>-Induced Differentiation in HaCaT Keratinocytes

Savignan¹,

Ballion²,

Odessa³

et al. 2004

J Biomed Sci

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We have used the human calcium- and temperature-dependent (HaCaT) keratinocyte cell line to elucidate mechanisms of switching from a proliferating to a differentiating state. When grown in low calcium medium (<0.1 mM) HaCaT cells proliferate. However, an increase in the calcium concentration of the culture medium, [Ca²⁺]₀, induces growth arrest and the cells start to differentiate. Numerous studies have already shown that the increase in [Ca²⁺]₀ results in acute and sustained increases in intracellular calcium concentration, [Ca²⁺]_i. We find that the Ca²⁺-induced cell differentiation of HaCaT cells is also accompanied by a significant decrease in mitochondrial membrane potential, DeltaPsi. By combining patch-clamp electrophysiological recordings and microspectrofluorimetric measurements of DeltaPsi on single cells, we show that the increase in [Ca²⁺]_i led to DeltaPsi depolarization. In addition, we report that tetraethylammonium (TEA), a blocker of plasma membrane K⁺ channels, which is known to inhibit cell proliferation, and 4,4’-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS), a blocker of plasma membrane Cl^– channels, also affect DeltaPsi. Both these agents stimulate HaCaT cell differentiation. These data therefore strongly suggest a direct causal relationship between depolarization of DeltaPsi and the inhibition of proliferation and induction of differentiation in HaCaT keratinocytes.

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“…According to the present results, T-SOD activity was significantly decreased in the NS, LD, and HD groups compared to the Sham group, but there was no remarkable difference among the NS, LD, and HD groups. On the basis of the study by Czyz et al [24]. and our present findings, we can further deduce that the ] can promote the recovery of mitochondrial function by improving the activity of ETC enzymes rather than via the ROS scavenging mechanism by SOD.…”

Section: Discussionmentioning

confidence: 59%

Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation

Qin

Xie

et al. 2018

Cell Physiol Biochem

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Background/Aims: The anti-apoptotic effect of an increase in the extracellular concentration of potassium ([K⁺]) has been confirmed in vitro. However, it is not yet known whether elevated serum [K⁺] exerts a cerebroprotective effect in vivo. In this study, we aimed to explore the effect of elevated serum [K⁺] in a rat model of middle cerebral artery occlusion and reperfusion (MCAO/R). Methods: Rats subjected to 90-min MCAO received 2.5% KCL, 1.25% KCL, or a normal saline solution at a dose of 3.2 mL/kg at the onset of reperfusion. Rats that were subjected to vascular exposure and ligation without MCAO were defined as the Sham group. Serum [K⁺] was determined using a blood gas analyzer at 1 min after medicine administration. At 24 h post-reperfusion, rat brains were harvested and processed for 2% 2,3,5-triphenyltetrazolium chloride staining, terminal deoxynucleotidyl transferase-mediated 2′-deoxyuridine 5′-triphosphate-biotin nick end labeling staining, detection of caspase-3 and cleaved-caspase-3 by western blotting, detection of reactive oxygen species (ROS) by dihydroethidium staining, and observation of mitochondrial structure by electron microscopy. In addition, malondialdehyde (MDA), adenosine triphosphate (ATP), total superoxide dismutase (T-SOD), cytochrome C oxidase (COX) activity, and mitochondrial permeability transition pore (MPTP) opening were measured using detection kits. Results: The results showed that elevated serum [K⁺] decreased cerebral injury and apoptosis, reduced ROS and MDA levels and MPTP opening, increased ATP levels and cytochrome C oxidase activity, and improved mitochondrial ultrastructural changes, although there was no significant difference in T-SOD activity. Conclusion: These findings suggested that elevated serum [K⁺] could alleviate cerebral ischemia-reperfusion injury and the mechanism may be associated with the preservation of mitochondrial function.

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The Role of Mitochondrial Potassium Fluxes in Controlling the Protonmotive Force in Energized Mitochondria

Cited by 50 publications

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Control Over the Contribution of the Mitochondrial Membrane Potential (ΔΨ) and Proton Gradient (ΔpH) to the Protonmotive Force (Δp)

Control Over the Contribution of the Mitochondrial Membrane Potential (ΔΨ) and Proton Gradient (ΔpH) to the Protonmotive Force (Δp)

Mitochondrial Membrane Potential (DeltaPsi) and Ca<sup>2+</sup>-Induced Differentiation in HaCaT Keratinocytes

Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation

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The Role of Mitochondrial Potassium Fluxes in Controlling the Protonmotive Force in Energized Mitochondria

Cited by 50 publications

References 0 publications

Control Over the Contribution of the Mitochondrial Membrane Potential (ΔΨ) and Proton Gradient (ΔpH) to the Protonmotive Force (Δp)

Control Over the Contribution of the Mitochondrial Membrane Potential (ΔΨ) and Proton Gradient (ΔpH) to the Protonmotive Force (Δp)

Mitochondrial Membrane Potential (DeltaPsi) and Ca<sup>2&plus;</sup>-Induced Differentiation in HaCaT Keratinocytes

Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation

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Mitochondrial Membrane Potential (DeltaPsi) and Ca<sup>2+</sup>-Induced Differentiation in HaCaT Keratinocytes