Aquaporin 2-increased renal cell proliferation is associated with cell volume regulation

2012 ◽  
Vol 113 (12) ◽  
pp. 3721-3729 ◽  
Author(s):  
Gisela Di Giusto ◽  
Pilar Flamenco ◽  
Valeria Rivarola ◽  
Juan Fernández ◽  
Luciana Melamud ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Volume ◽  
Renal Cell ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Aquaporin 2

scholarly journals NAD(P)H Oxidase-derived H2O2Signals Chloride Channel Activation in Cell Volume Regulation and Cell Proliferation

2004 ◽  
Vol 279 (14) ◽  
pp. 13301-13304 ◽  
Author(s):  
Diego Varela ◽  
Felipe Simon ◽  
Ana Riveros ◽  
Finn Jørgensen ◽  
Andrés Stutzin
Keyword(s):  
Cell Proliferation ◽  
Cell Volume ◽  
Chloride Channel ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Channel Activation

On the role of TRPC1 in control of Ca2+ influx, cell volume, and cell cycle

2012 ◽  
Vol 303 (6) ◽  
pp. C625-C634 ◽  
Author(s):  
C. P. Madsen ◽  
T. K. Klausen ◽  
A. Fabian ◽  
B. J. Hansen ◽  
S. F. Pedersen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Cycle Progression ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
S Phase ◽  
Cycle Progression

Ca+ signaling plays a crucial role in control of cell cycle progression, but the understanding of the dynamics of Ca2+ influx and release of Ca2+ from intracellular stores during the cell cycle is far from complete. The aim of the present study was to investigate the role of the free extracellular Ca2+ concentration ([Ca2+]o) in cell proliferation, the pattern of changes in the free intracellular Ca2+ concentration ([Ca2+]i) during cell cycle progression, and the role of the transient receptor potential (TRP)C1 in these changes as well as in cell cycle progression and cell volume regulation. In Ehrlich Lettré Ascites (ELA) cells, [Ca2+]i decreased significantly, and the thapsigargin-releasable Ca2+ pool in the intracellular stores increased in G1 as compared with G0. Store-depletion-operated Ca2+ entry (SOCE) and TRPC1 protein expression level were both higher in G1 than in G0 and S phase, in parallel with a more effective volume regulation after swelling [regulatory volume decrease (RVD)] in G1 as compared with S phase. Furthermore, reduction of [Ca2+]o, as well as two unspecific SOCE inhibitors, 2-APB (2-aminoethyldiphenyl borinate) and SKF96365 (1-(β-[3-(4-methoxy-phenyl)propoxyl-4-methoxyphenethyl)1H-imidazole-hydrochloride), inhibited ELA cell proliferation. Finally, Madin-Darby canine kidney cells in which TRPC1 was stably silenced [TRPC1 knockdown (TRPC1-KD) MDCK] exhibited reduced SOCE, slower RVD, and reduced cell proliferation compared with mock controls. In conclusion, in ELA cells, SOCE and TRPC1 both seem to be upregulated in G1 as compared with S phase, concomitant with an increased rate of RVD. Furthermore, TRPC1-KD MDCK cells exhibit decreased SOCE, decreased RVD, and decreased proliferation, suggesting that, at least in certain cell types, TRPC1 is regulated during cell cycle progression and is involved in SOCE, RVD, and cell proliferation.

Mechanisms responsible for cell volume regulation during hyperkalemic cardioplegic arrest

2000 ◽  
Vol 70 (2) ◽  
pp. 633-638
Author(s):  
Xiwu Sun ◽  
Christopher T Ducko ◽  
Eric M Hoenicke ◽  
Karen Reigle ◽  
Ralph J Damiano
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Cardioplegic Arrest
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