Cell Volume Regulatory Ion Transport in the Regulation of Cell Migration

2006 ◽  
pp. 161-180 ◽  
Author(s):  
M. Jakab ◽  
M. Ritter
Keyword(s):  
Cell Migration ◽  
Ion Transport ◽  
Cell Volume

Hyperosmotic and isosmotic shrinkage differentially affect protein phosphorylation and ion transport

2012 ◽  
Vol 90 (2) ◽  
pp. 209-217 ◽  
Author(s):  
Svetlana V. Koltsova ◽  
Olga A. Akimova ◽  
Sergei V. Kotelevtsev ◽  
Ryszard Grygorczyk ◽  
Sergei N. Orlov
Keyword(s):  
Ion Transport ◽  
Protein Phosphorylation ◽  
Cell Volume ◽  
Mdck Cells ◽  
Rat Aorta ◽  
Cellular Functions ◽  
Hypertonic Medium ◽  
Mitogen Activated Protein ◽  
Volume Decrease ◽  
In Cells

In the present work, we compared the outcome of hyperosmotic and isosmotic shrinkage on ion transport and protein phosphorylation in C11-MDCK cells resembling intercalated cells from collecting ducts and in vascular smooth muscle cells (VSMC) from the rat aorta. Hyperosmotic shrinkage was triggered by cell exposure to hypertonic medium, whereas isosmotic shrinkage was evoked by cell transfer from an hypoosmotic to an isosmotic environment. Despite a similar cell volume decrease of 40%–50%, the consequences of hyperosmotic and isosmotic shrinkage on cellular functions were sharply different. In C11-MDCK and VSMC, hyperosmotic shrinkage completely inhibited Na+,K+-ATPase and Na+,Pi cotransport. In contrast, in both types of cells isosmotic shrinkage slightly increased rather than suppressed Na+,K+-ATPase and did not change Na+,Pi cotransport. In C11-MDCK cells, phosphorylation of JNK1/2 and Erk1/2 mitogen-activated protein kinases was augmented in hyperosmotically shrunken cells by ∼7- and 2-fold, respectively, but was not affected in cells subjected to isosmotic shrinkage. These results demonstrate that the data obtained in cells subjected to hyperosmotic shrinkage cannot be considered as sufficient proof implicating cell volume perturbations in the regulation of cellular functions under isosmotic conditions.

Restitution of the bullfrog gastric mucosa is dependent on a DIDS-inhibitable pathway not related to \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{HCO}_{3}^{-}\) \end{document} ion transport

2004 ◽  
Vol 286 (4) ◽  
pp. G596-G605 ◽  
Author(s):  
Susan J. Hagen ◽  
Sarah W. Morrison ◽  
Christina S. Law ◽  
David X. Yang
Keyword(s):  
Cell Migration ◽  
Gastric Mucosa ◽  
Basement Membrane ◽  
Ion Transport ◽  
Rana Catesbeiana ◽  
Transepithelial Resistance ◽  
Ussing Chambers ◽  
Ion Substitution ◽  
Transport Inhibitors ◽  
Mannitol Flux

This study was conducted to determine the contribution of ion transport to restitution after injury in the gastric mucosa. For this, intact sheets of stomach from the bullfrog, Rana catesbeiana, were mounted in Ussing chambers. Restitution was evaluated in the presence or absence of ion transport inhibitors amiloride, DIDS, and bumetanide to block Na+/H+ exchange, [Formula: see text]/[Formula: see text] exchange and [Formula: see text]/[Formula: see text] co-transport, and Na+-K+-2Cl- cotransport, respectively. Ion substitution experiments with Na+-free, Cl--free, and [Formula: see text]-free solutions were also performed. Injury to the mucosa was produced with 1 M NaCl, and restitution was evaluated by recovery of transepithelial resistance (TER), mannitol flux, and morphology. Amiloride, bumetanide, Cl--free, or [Formula: see text]-free solutions did not affect restitution. In Na+-free solutions, recovery of TER and mannitol flux did not occur because surface cells did not attach to the underlying basement membrane. In contrast, all aspects of restitution were inhibited by DIDS, a compound that inhibits Na+-dependent [Formula: see text] transport. Because [Formula: see text]-free solutions did not inhibit restitution, it was concluded that DIDS must block a yet undefined pathway not involved in [Formula: see text] ion transport but essential for cell migration after injury and restitution in the gastric mucosa.

Regulation of intracellular pH in alveolar epithelial cells

1992 ◽  
Vol 262 (1) ◽  
pp. L1-L14 ◽  
Author(s):  
R. L. Lubman ◽  
E. D. Crandall
Keyword(s):  
Epithelial Cells ◽  
Ion Transport ◽  
Cell Volume ◽  
Intracellular Ph ◽  
Type I ◽  
Transport Mechanisms ◽  
Alveolar Epithelial ◽  
Cellular Processes ◽  
Proliferation And Differentiation ◽  
Phi Regulation

Alveolar type II epithelial cells in adult mammalian lungs actively transport salt and water, secrete surfactant, and differentiate into type I cells under normal conditions and following lung injury. It has become increasingly apparent that, like all epithelial cells, alveolar pneumocytes have evolved specialized ion transport mechanisms by which they regulate their intracellular pH (pHi). pHi is an important biological parameter in all living cells whose regulation is necessary for normal cellular homeostasis. pHi, and the ion transport mechanisms by which it is regulated, may contribute to many cellular processes, including transcellular transport, cell volume and osmolarity regulation, and intracellular transport, cell volume and osmolarity regulation, and intracellular electrolyte composition. Moreover, changes in pHi may serve as intracellular signals for biological processes such as cell growth, proliferation, and differentiation. We review herein the general principles of pHi regulation in epithelia and describe the mechanisms and effects of pHi regulation in alveolar pneumocytes. Many of the critical issues in current pulmonary research involve processes that pHi is most likely to affect, including maintenance of alveolar epithelial barrier integrity, development and maintenance of epithelial polarity, epithelial proliferation and differentiation, and regulation of transepithelial transport with respect to alveolar fluid balance in normal individuals and in those with excess alveolar fluid (i.e., pulmonary edema). Investigations into the regulation of pHi in alveolar pneumocytes and the regulatory effects of pHi in turn on other cellular processes are likely to yield information important to the understanding of lung biology and pulmonary disease.

scholarly journals Cardiac Glycoside Activities Link Na+/K+ATPase Ion-Transport to Breast Cancer Cell Migration via Correlative SAR

2014 ◽  
Vol 10 (2) ◽  
pp. 561-569 ◽  
Author(s):  
Anniefer N. Magpusao ◽  
George Omolloh ◽  
Joshua Johnson ◽  
José Gascón ◽  
Mark W. Peczuh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Ion Transport ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cardiac Glycoside ◽  
Cancer Cell Migration ◽  
Breast Cancer Cell Migration

scholarly journals Ion channels and transporters in tumour cell migration and invasion

2014 ◽  
Vol 369 (1638) ◽  
pp. 20130102 ◽  
Author(s):  
Albrecht Schwab ◽  
Christian Stock
Keyword(s):  
Cell Migration ◽  
Ion Channels ◽  
Ion Transport ◽  
Tumour Cell ◽  
Transport Proteins ◽  
Migration And Invasion ◽  
Central Component ◽  
Cell Migration And Invasion ◽  
Candidate Target ◽  
Cytoskeletal Elements

Cell migration is a central component of the metastatic cascade requiring a concerted action of ion channels and transporters (migration-associated transportome), cytoskeletal elements and signalling cascades. Ion transport proteins and aquaporins contribute to tumour cell migration and invasion among other things by inducing local volume changes and/or by modulating Ca 2+ and H + signalling. Targeting cell migration therapeutically bears great clinical potential, because it is a prerequisite for metastasis. Ion transport proteins appear to be attractive candidate target proteins for this purpose because they are easily accessible as membrane proteins and often overexpressed or activated in cancer. Importantly, a number of clinically widely used drugs are available whose anticipated efficacy as anti-tumour drugs, however, has now only begun to be evaluated.

Cellular osmoregulation: beyond ion transport and cell volume

Zoology ◽  
2001 ◽  
Vol 104 (3-4) ◽  
pp. 198-208 ◽  
Author(s):  
Dietmar Kültz
Keyword(s):  
Ion Transport ◽  
Cell Volume

scholarly journals The Important Role of Ion Transport System in Cervical Cancer

2021 ◽  
Vol 23 (1) ◽  
pp. 333
Author(s):  
Yih-Fung Chen ◽  
Meng-Ru Shen
Keyword(s):  
Cervical Cancer ◽  
Epithelial Cells ◽  
Ion Transport ◽  
Cell Volume ◽  
Volume Regulation ◽  
Gynecological Cancer ◽  
Cell Volume Regulation ◽  
Hpv Infection ◽  
Transport Processes ◽  
Transport Systems

Cervical cancer is a significant gynecological cancer and causes cancer-related deaths worldwide. Human papillomavirus (HPV) is implicated in the etiology of cervical malignancy. However, much evidence indicates that HPV infection is a necessary but not sufficient cause in cervical carcinogenesis. Therefore, the cellular pathophysiology of cervical cancer is worthy of study. This review summarizes the recent findings concerning the ion transport processes involved in cell volume regulation and intracellular Ca2+ homeostasis of epithelial cells and how these transport systems are themselves regulated by the tumor microenvironment. For cell volume regulation, we focused on the volume-sensitive Cl− channels and K+-Cl− cotransporter (KCC) family, important regulators for ionic and osmotic homeostasis of epithelial cells. Regarding intracellular Ca2+ homeostasis, the Ca2+ store sensor STIM molecules and plasma membrane Ca2+ channel Orai proteins, the predominant Ca2+ entry mechanism in epithelial cells, are discussed. Furthermore, we evaluate the potential of these membrane ion transport systems as diagnostic biomarkers and pharmacological interventions and highlight the challenges.

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