Physiological implications of the regulation of vacuolar H+-ATPase by chloride ions

Carraro‐Lacroix, Luciene Regina; Lessa, Lucília Maria Abreu; Fernández, Ricardo; Malnic, Gerhard

doi:10.1590/s0100-879x2009000200002

Cited by 17 publications

(18 citation statements)

References 56 publications

(81 reference statements)

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“…This raises the activity of V-ATPase, which consequently increases the concentration of H + within the organelles [185]. Acidification of the interior favors the accumulation of protonated forms of amino-containing weak bases.…”

Section: Vacuolization and Unknown Cell Death Pathwaysmentioning

confidence: 99%

Cytoplasmic vacuolization in cell death and survival

et al. 2016

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Cytoplasmic vacuolization (also called cytoplasmic vacuolation) is a well-known morphological phenomenon observed in mammalian cells after exposure to bacterial or viral pathogens as well as to various natural and artificial low-molecular-weight compounds. Vacuolization often accompanies cell death; however, its role in cell death processes remains unclear. This can be attributed to studying vacuolization at the level of morphology for many years. At the same time, new data on the molecular mechanisms of the vacuole formation and structure have become available. In addition, numerous examples of the association between vacuolization and previously unknown cell death types have been reported. Here, we review these data to make a deeper insight into the role of cytoplasmic vacuolization in cell death and survival.

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Section: Vacuolization and Unknown Cell Death Pathwaysmentioning

confidence: 99%

Cytoplasmic vacuolization in cell death and survival

et al. 2016

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“…Impaired chloride transport can cause a variety of diseases such as cystic fibrosis, myotonia, epilepsy, hyperekplexia, lysosomal storage disease, deafness, renal salt loss, kidney stones, and osteopetrosis [1,2,[4][5][6][7][8][9][10]. Several major classes of chloride channels have been defined based on structural or functional differences: ligandgated chloride channels, cystic fibrosis transmembrane conductance regulators (CFTRs), the intracellular chloride channel (CLIC), voltage-gated chloride channels (ClCs) and calcium-activated chloride channels [2,[11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial chloride channels – What are they for?

Tomaskova

Ondriaš

2010

FEBS Letters

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a b s t r a c tThis minireview focuses on observation of the properties, functional significance, and modulation of single chloride channels in the mitochondrial inner membrane using two electrophysiological methods -the patch-clamp and bilayer lipid membrane methods. Measurements of parameters such as conductance, Cl À /K + selectivity, voltage or pH dependence as well as their modulation by endogenous and exogenous compounds using individual mitochondrial chloride channels result in an unexpectedly wide range of values. This paper discusses the origin of this wide variety of channel parameters and the possible involvement of these channels in mitochondrial membrane potential oscillations, apoptosis, carrier function, and mitochondrial fusion and fission.

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“…It has been accepted that chloride ions moving along chloride conductances act to dissipate the electrical gradient established by the electrogenic transport of H + ions performed by H + -ATPase into subcellular vesicles or to the cell surface [3,46]. Several lines of evidence for this interaction have been observed so far supporting this view, including a number of studies from our research group [8,21,22,28].…”

Section: Discussionmentioning

confidence: 85%

Role of CFTR and ClC-5 in Modulating Vacuolar H<sup>+</sup>-ATPase Activity in Kidney Proximal Tubule

Carraro‐Lacroix

Lessa

Bezerra

et al. 2010

Cell Physiol Biochem

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Background/Aims: It has been widely accepted that chloride ions moving along chloride channels act to dissipate the electrical gradient established by the electrogenic transport of H⁺ ions performed by H⁺-ATPase into subcellular vesicles. Largely known in intracellular compartments, this mechanism is also important at the plasma membrane of cells from various tissues, including kidney. The present work was performed to study the modulation of plasma membrane H⁺-ATPase by chloride channels, in particular, CFTR and ClC-5 in kidney proximal tubule. Methods and Results: Using in vivo stationary microperfusion, it was observed that ATPase-mediated HCO₃^- reabsorption was significantly reduced in the presence of the Cl^- channels inhibitor NPPB. This effect was confirmed in vitro by measuring the cell pH recovery rates after a NH₄Cl pulse in immortalized rat renal proximal tubule cells, IRPTC. In these cells, even after abolishing the membrane potential with valinomycin, ATPase activity was seen to be still dependent on Cl^-. siRNA-mediated CFTR channels and ClC-5 chloride-proton exchanger knockdown significantly reduced H⁺-ATPase activity and V-ATPase B2 subunit expression. Conclusion: These results indicate a role of chloride in modulating plasma membrane H⁺-ATPase activity in proximal tubule and suggest that both CFTR and ClC-5 modulate ATPase activity.

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Physiological implications of the regulation of vacuolar H+-ATPase by chloride ions

Cited by 17 publications

References 56 publications

Cytoplasmic vacuolization in cell death and survival

Cytoplasmic vacuolization in cell death and survival

Mitochondrial chloride channels – What are they for?

Role of CFTR and ClC-5 in Modulating Vacuolar H<sup>+</sup>-ATPase Activity in Kidney Proximal Tubule

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