scholarly journals Receptor-Mediated Facilitation of Cell Volume Regulation by Swelling-Induced ATP Release in Human Epithelial Cells.

2000 ◽  
Vol 50 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Katsuya Dezaki ◽  
Takehiko Tsumura ◽  
Emi Maeno ◽  
Yasunobu Okada
2000 ◽  
Vol 118 (4) ◽  
pp. A239
Author(s):  
Outi Nylander-Koski ◽  
Harri Mustonen ◽  
Tuula Kiviluoto ◽  
Eero Kivilaakso

1999 ◽  
Vol 276 (6) ◽  
pp. G1391-G1400 ◽  
Author(s):  
Richard M. Roman ◽  
Andrew P. Feranchak ◽  
Kelli D. Salter ◽  
Yu Wang ◽  
J. Gregory Fitz

P2Y receptor stimulation increases membrane Cl− permeability in biliary epithelial cells, but the source of extracellular nucleotides and physiological relevance of purinergic signaling to biliary secretion are unknown. Our objectives were to determine whether biliary cells release ATP under physiological conditions and whether extracellular ATP contributes to cell volume regulation and transepithelial secretion. With the use of a sensitive bioluminescence assay, constitutive ATP release was detected from human Mz-ChA-1 cholangiocarcinoma cells and polarized normal rat cholangiocyte monolayers. ATP release increased rapidly during cell swelling induced by hypotonic exposure. In Mz-ChA-1 cells, removal of extracellular ATP (apyrase) and P2 receptor blockade (suramin) reversibly inhibited whole cell Cl− current activation and prevented cell volume recovery during hypotonic stress. Moreover, exposure to apyrase induced cell swelling under isotonic conditions. In intact normal rat cholangiocyte monolayers, hypotonic perfusion activated apical Cl−currents, which were inhibited by addition of apyrase and suramin to bathing media. These findings indicate that modulation of ATP release by the cellular hydration state represents a potential signal coordinating cell volume with membrane Cl− permeability and transepithelial Cl−secretion.


2011 ◽  
Vol 436 (1) ◽  
pp. 13-15 ◽  
Author(s):  
E. I. Solenov ◽  
G. S. Baturina ◽  
A. V. Ilyaskin ◽  
L. Ye. Katkova ◽  
L. N. Ivanova

1998 ◽  
Vol 273 (24) ◽  
pp. 14906-14911 ◽  
Author(s):  
Andrew P. Feranchak ◽  
Richard M. Roman ◽  
Erik M. Schwiebert ◽  
J. Gregory Fitz

2021 ◽  
Vol 23 (1) ◽  
pp. 333
Author(s):  
Yih-Fung Chen ◽  
Meng-Ru Shen

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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