scholarly journals Role of adenosine on glucagon-induced cAMP in a human cortical collecting duct cell line

1995 ◽  
Vol 47 (5) ◽  
pp. 1310-1318 ◽  
Author(s):  
Dominique Prié ◽  
Gérard Friedlander ◽  
Christiane Coureau ◽  
Alain Vandewalle ◽  
Roland Cassingéna ◽  
...  
2005 ◽  
Vol 207 (3) ◽  
pp. 143-150 ◽  
Author(s):  
O. Chara ◽  
P. Ford ◽  
V. Rivarola ◽  
M. Parisi ◽  
C. Capurro

2002 ◽  
Vol 190 (2) ◽  
pp. 117-125 ◽  
Author(s):  
P. Ford ◽  
V. Rivarola ◽  
A. Kierbel ◽  
O. Chara ◽  
M. Blot-Chabaud ◽  
...  

2004 ◽  
Vol 19 (5) ◽  
pp. 1069-1076 ◽  
Author(s):  
J. C. de Jong ◽  
P. H. G. M. Willems ◽  
M. Goossens ◽  
A. Vandewalle ◽  
L. P. W. J. van den Heuvel ◽  
...  

2002 ◽  
Vol 282 (3) ◽  
pp. F541-F552 ◽  
Author(s):  
Bradley K. Yoder ◽  
Albert Tousson ◽  
Leigh Millican ◽  
John H. Wu ◽  
Charles E. Bugg ◽  
...  

Cilia are organelles that play diverse roles, from fluid movement to sensory reception. Polaris, a protein associated with cystic kidney disease in Tg737°rpkmice, functions in a ciliogenic pathway. Here, we explore the role of polaris in primary cilia on Madin-Darby canine kidney cells. The results indicate that polaris localization and solubility change dramatically during cilia formation. These changes correlate with the formation of basal bodies and large protein rafts at the apical surface of the epithelia. A cortical collecting duct cell line has been derived from mice with a mutation in the Tg737 gene. These cells do not develop normal cilia, which can be corrected by reexpression of the wild-type Tg737 gene. These data suggest that the primary cilia are important for normal renal function and/or development and that the ciliary defect may be a contributing factor to the cystic disease in Tg737°rpkmice. Further characterization of these cells will be important in elucidating the physiological role of renal cilia and in determining their relationship to cystic disease.


2001 ◽  
Vol 98 (5) ◽  
pp. 2712-2716 ◽  
Author(s):  
M. Robert-Nicoud ◽  
M. Flahaut ◽  
J.-M. Elalouf ◽  
M. Nicod ◽  
M. Salinas ◽  
...  

2001 ◽  
Vol 179 (1) ◽  
pp. 63-70 ◽  
Author(s):  
C. Capurro ◽  
V. Rivarola ◽  
A. Kierbel ◽  
B. Escoubet ◽  
N. Farman ◽  
...  

2003 ◽  
Vol 104 (3) ◽  
pp. 217-221 ◽  
Author(s):  
Kimberly M. HOOPER ◽  
Robert J. UNWIN ◽  
Michael SUTTERS

Cyst expansion in autosomal dominant polycystic kidney disease (ADPKD) requires accumulation of fluid into the cyst lumen, which is probably driven by aberrant chloride secretion by the cyst lining epithelium. Extracellular ATP is a potent stimulus for chloride secretion in many epithelial systems, and provides a plausible mechanism for secretion in ADPKD. Therefore the link between polycystin-1 and ATP-stimulated chloride secretion was investigated in the M1 cortical collecting duct cell line. M1 cells were stably transfected with a glucocorticoid-inducible cytoplasmic C-terminal polycystin-1 construct fused to a membrane expression cassette. Induction of fusion protein expression was associated with augmentation of ATP-stimulated transepithelial chloride secretion. After nystatin-induced permeabilization of the basolateral membrane, it was determined that expression of the polycystin fusion protein modulated an ATP-responsive apical chloride conductance. It is concluded that up-regulation of ATP-stimulated chloride secretion might play a significant role in cyst expansion in ADPKD.


1997 ◽  
Vol 51 (1) ◽  
pp. 281-287 ◽  
Author(s):  
Valerie Millul ◽  
Nicole Ardaillou ◽  
Sandrine Placier ◽  
Béatrice Baudouin ◽  
Pierre M. Ronco

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