scholarly journals Ouabain-Induced Cytoplasmic Vesicles and Their Role in Cell Volume Maintenance

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
M. A. Russo ◽  
E. Morgante ◽  
A. Russo ◽  
G. D. van Rossum ◽  
M. Tafani

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.

2020 ◽  
Vol 118 (3) ◽  
pp. 461a
Author(s):  
Maria Jesus Munoz Lopez ◽  
Yoichiro Mori

1996 ◽  
pp. 2015-2031 ◽  
Author(s):  
A. R. Taylor ◽  
NFH. Manison ◽  
C. Fernandez ◽  
J. Wood ◽  
C. Brownlee

1998 ◽  
Vol 331 (3) ◽  
pp. 863-869 ◽  
Author(s):  
Thea van Der WIJK ◽  
Jannette DORRESTIJN ◽  
Shuh NARUMIYA ◽  
J. Antonie MAASSEN ◽  
Hugo R. De JONGE ◽  
...  

Human Intestine 407 cells respond to hypo-osmotic stress with a rapid stimulation of compensatory ionic conductances accompanied by a transient increase in the activity of the extracellular-signal-regulated protein kinases Erk-1 and Erk-2. In this study, we examined the upstream regulators of hypotonicity-induced Erk-1/Erk-2 activation and their possible role in cell-volume regulation. The hypotonicity-provoked Erk-1/Erk-2 activation was greatly reduced in cells pretreated with the specific mitogen-activated/Erk-activating kinase inhibitor PD098059 and was preceded by a transient stimulation of Raf-1. Pretreatment of the cells with PMA, GF 109203X, wortmannin or Clostridium botulinum C3 exoenzyme did not appreciably affect the hypotonicity-provoked Erk-1/Erk-2 stimulation, suggesting the osmosensitive signalling pathway to be largely independent of protein kinase C and p21rho. In contrast, expression of dominant negative RasN17 completely abolished the hypotonicity-induced Erk-1/Erk-2 activation. Stimulation of the swelling-induced ion efflux was independent of activation of these mitogen-activated protein kinases, as revealed by hypotonicity-provoked isotope efflux from 125I-- and 86Rb+-loaded cells after pretreatment with PD098059 and after expression of RasN17. In addition, the epidermal-growth-factor-induced potentiation of the hypotonicity-provoked anionic response did not depend on the increase in Erk-1/Erk-2 activity but, instead, was found to depend on Ca2+ influx. Taken together, these results indicate that hypotonic stress induces Erk-1/Erk-2 activation through the Ras/Raf-signalling pathway, and argue against a direct role for this pathway in cell-volume control.


2008 ◽  
pp. 69-105
Author(s):  
Richard D. Allen ◽  
Takashi Tominaga ◽  
Yutaka Naitoh

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