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Ouabain-induced cytoplasmic vesicles and their role in cell volume maintenance.

Russo MA, Morgante E, Russo A, van Rossum GD, Tafani M - Biomed Res Int (2015)

Bottom Line: Na(+)/K(+)-pump may be blocked by ouabain, a digitalic derivative, by inhibition of ATP, or by drastic ion alterations of extracellular fluid.In particular, hepatocytes were able to sequester ions and water in intracellular vesicles and then secrete them at the bile canaliculus pole.This review summarizes evidences regarding this mechanism, problems that are still pending, and questions that need to be answered.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Molecular and Cellular Pathology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Roma, Italy.

ABSTRACT
Cellular swelling is controlled by an active mechanism of cell volume regulation driven by a Na(+)/K(+)-dependent ATPase and by aquaporins which translocate water along the osmotic gradient. Na(+)/K(+)-pump may be blocked by ouabain, a digitalic derivative, by inhibition of ATP, or by drastic ion alterations of extracellular fluid. However, it has been observed that some tissues are still able to control their volume despite the presence of ouabain, suggesting the existence of other mechanisms of cell volume control. In 1977, by correlating electron microscopy observation with ion and water composition of liver slices incubated in different metabolic conditions in the presence or absence of ouabain, we observed that hepatocytes were able to control their volume extruding water and recovering ion composition in the presence of ouabain. In particular, hepatocytes were able to sequester ions and water in intracellular vesicles and then secrete them at the bile canaliculus pole. We named this "vesicular mechanism of cell volume control." Afterward, this mechanism has been confirmed by us and other laboratories in several mammalian tissues. This review summarizes evidences regarding this mechanism, problems that are still pending, and questions that need to be answered. Finally, we shortly review the importance of cell volume control in some human pathological conditions.

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Schematic representation of the ouabain-resistant mechanism of cell volume control, the origin of vesicles, their secretion, and the effects of metabolic inhibitors. CCCP = carbonyl cyanide m-chlorophenylhydrazone; DCCD = N,N′-dicyclohexylcarbodiimide.
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fig9: Schematic representation of the ouabain-resistant mechanism of cell volume control, the origin of vesicles, their secretion, and the effects of metabolic inhibitors. CCCP = carbonyl cyanide m-chlorophenylhydrazone; DCCD = N,N′-dicyclohexylcarbodiimide.

Mentions: Briefly (see also Figure 9), formation of the vesicles is dependent on the presence of Cl−. Vesicles appear to originate by expansion of terminal cisternae of the endoplasmic reticulum and of Golgi elements and they have an acidic content. In liver, the vesicles accumulate and secrete at the canalicular pole and in renal cortex near the basolateral infolding of the plasma membrane. In each case and most clearly in the kidney, there is evidence of their fusion with the plasma membrane suggesting expulsion of the content [18, 24].


Ouabain-induced cytoplasmic vesicles and their role in cell volume maintenance.

Russo MA, Morgante E, Russo A, van Rossum GD, Tafani M - Biomed Res Int (2015)

Schematic representation of the ouabain-resistant mechanism of cell volume control, the origin of vesicles, their secretion, and the effects of metabolic inhibitors. CCCP = carbonyl cyanide m-chlorophenylhydrazone; DCCD = N,N′-dicyclohexylcarbodiimide.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4383472&req=5

fig9: Schematic representation of the ouabain-resistant mechanism of cell volume control, the origin of vesicles, their secretion, and the effects of metabolic inhibitors. CCCP = carbonyl cyanide m-chlorophenylhydrazone; DCCD = N,N′-dicyclohexylcarbodiimide.
Mentions: Briefly (see also Figure 9), formation of the vesicles is dependent on the presence of Cl−. Vesicles appear to originate by expansion of terminal cisternae of the endoplasmic reticulum and of Golgi elements and they have an acidic content. In liver, the vesicles accumulate and secrete at the canalicular pole and in renal cortex near the basolateral infolding of the plasma membrane. In each case and most clearly in the kidney, there is evidence of their fusion with the plasma membrane suggesting expulsion of the content [18, 24].

Bottom Line: Na(+)/K(+)-pump may be blocked by ouabain, a digitalic derivative, by inhibition of ATP, or by drastic ion alterations of extracellular fluid.In particular, hepatocytes were able to sequester ions and water in intracellular vesicles and then secrete them at the bile canaliculus pole.This review summarizes evidences regarding this mechanism, problems that are still pending, and questions that need to be answered.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Molecular and Cellular Pathology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Roma, Italy.

ABSTRACT
Cellular swelling is controlled by an active mechanism of cell volume regulation driven by a Na(+)/K(+)-dependent ATPase and by aquaporins which translocate water along the osmotic gradient. Na(+)/K(+)-pump may be blocked by ouabain, a digitalic derivative, by inhibition of ATP, or by drastic ion alterations of extracellular fluid. However, it has been observed that some tissues are still able to control their volume despite the presence of ouabain, suggesting the existence of other mechanisms of cell volume control. In 1977, by correlating electron microscopy observation with ion and water composition of liver slices incubated in different metabolic conditions in the presence or absence of ouabain, we observed that hepatocytes were able to control their volume extruding water and recovering ion composition in the presence of ouabain. In particular, hepatocytes were able to sequester ions and water in intracellular vesicles and then secrete them at the bile canaliculus pole. We named this "vesicular mechanism of cell volume control." Afterward, this mechanism has been confirmed by us and other laboratories in several mammalian tissues. This review summarizes evidences regarding this mechanism, problems that are still pending, and questions that need to be answered. Finally, we shortly review the importance of cell volume control in some human pathological conditions.

Show MeSH
Related in: MedlinePlus