The isolated C-terminus of polycystin-1 promotes increased ATP-stimulated chloride secretion in a collecting duct cell line

2003 ◽  
Vol 104 (3) ◽  
pp. 217 ◽  
Author(s):  
Kimberly M. HOOPER ◽  
Robert J. UNWIN ◽  
Michael SUTTERS
Keyword(s):  
Cell Line ◽  
Collecting Duct ◽  
Duct Cell ◽  
Chloride Secretion ◽  
C Terminus

The isolated C-terminus of polycystin-1 promotes increased ATP-stimulated chloride secretion in a collecting duct cell line

2003 ◽  
Vol 104 (3) ◽  
pp. 217-221 ◽  
Author(s):  
Kimberly M. HOOPER ◽  
Robert J. UNWIN ◽  
Michael SUTTERS
Keyword(s):  
Fusion Protein ◽  
Cell Line ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Duct Cell ◽  
Chloride Secretion ◽  
Cortical Collecting Duct ◽  
Membrane Expression ◽  
Fusion Protein Expression ◽  
C Terminus

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.

Adenosine inhibits arginine vasopressin-stimulated chloride secretion in a mouse IMCD cell line (mIMCD-K2)

1995 ◽  
Vol 269 (6) ◽  
pp. F884-F891 ◽  
Author(s):  
B. D. Moyer ◽  
D. E. McCoy ◽  
B. Lee ◽  
N. Kizer ◽  
B. A. Stanton
Keyword(s):  
Cell Line ◽  
Arginine Vasopressin ◽  
Collecting Duct ◽  
Duct Cell ◽  
Chloride Secretion ◽  
Nucleoside Transport ◽  
Intracellular Camp ◽  
Nucleoside Transporter ◽  
Cl Channels ◽  
Medullary Collecting Duct

Previously, we demonstrated that a mouse inner medullary collecting duct cell line (mIMCD-K2) secretes Cl- by an electrogenic mechanism via cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels [N. L. Kizer, B. Lewis, and B. A. Stanton. Am. J. Physiol. 268 (Renal Fluid Electrolyte Physiol. 37): F347-F355, 1995; N. L. Kizer, D. Vandorpe, B. Lewis, B. Bunting, J. Russell, and B. A. Stanton. Am. J. Physiol. 268 (Renal Fluid Electrolyte Physiol. 37): F854-F861, 1995; D. Vandorpe, N. Kizer, F. Ciampolillo-Bates, B. Moyer, K. Karlson, W. B. Guggino, and B. A. Stanton. Am. J. Physiol. 269 (Cell Physiol. 38): C683-C689, 1995]. The objective of the present study was to determine whether adenosine, and adenosine A1 receptors (A1AR) specifically, regulate electrogenic Cl- secretion (IscCl) in mIMCD-K2 cells. Neither N6-cyclohexyladenosine (CHA), a specific A1AR agonist, nor 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a specific A1AR antagonist, altered basal, unstimulated IscCl in monolayers of mIMCD-K2 cells mounted in Ussing-type chambers. In contrast, DPCPX increased arginine vasopressin (AVP)-stimulated IscCl, an effect that was reversed by CHA. Adenosine deaminase (ADA), which oxidatively deaminates adenosine to inosine, increased AVP-stimulated IscCl. CHA reversed the stimulatory effect of ADA on AVP-stimulated IscCl. These results suggest that adenosine, via A1AR, inhibits AVP-stimulated IscCl. To identify the source(s) of extracellular adenosine, we examined the effects of dipyridamole, an inhibitor of nucleoside transport, and alpha,beta-methyleneadenosine 5'-diphosphate (AOPCP), an inhibitor of ecto-5'-nucleotidase, on AVP-stimulated IscCl. Both compounds increased AVP-stimulated IscCl. CHA reversed the stimulatory effect of dipyridamole and AOPCP on IscCl. Neither ADA nor CHA had an effect on 8-(4-chlorophenylthio)-adenosine 3',5'-cyclic monophosphate (CPT-cAMP)-stimulated IscCl. Moreover, U-73122, an inhibitor of phospholipase C, failed to attenuate the increase in AVP-stimulated IscCl elicited by dipyridamole and AOPCP or the decrease in AVP-stimulated IscCl elicited by CHA. We conclude that adenosine, released by a nucleoside transporter and formed extracellularly by the breakdown of AMP, binds to A1AR, and decreases AVP-stimulated IscCl in mIMCD-K2 cells by reducing intracellular cAMP levels.

scholarly journals Effects of chemical chaperones on partially retarded NaCl cotransporter mutants associated with Gitelman's syndrome in a mouse cortical collecting duct cell line

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 ◽  
...  
Keyword(s):  
Cell Line ◽  
Collecting Duct ◽  
Duct Cell ◽  
Cortical Collecting Duct ◽  
Chemical Chaperones ◽  
Gitelman's Syndrome ◽  
Nacl Cotransporter

Early transcriptional effects of aldosterone in a mouse inner medullary collecting duct cell line

2003 ◽  
Vol 285 (4) ◽  
pp. F664-F673 ◽  
Author(s):  
Michelle L. Gumz ◽  
Michael P. Popp ◽  
Charles S. Wingo ◽  
Brian D. Cain
Keyword(s):  
Cell Line ◽  
Cellular Response ◽  
Collecting Duct ◽  
Duct Cell ◽  
Immunoblot Analysis ◽  
Tissue Growth ◽  
Long Term Effects ◽  
Acid Base Balance ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

The mineralocorticoid aldosterone is a major regulator of Na+ and acid-base balance and control of blood pressure. Although the long-term effects of aldosterone have been extensively studied, the early aldosterone-responsive genes remain largely unknown. Using DNA array technology, we have characterized changes in gene expression after 1 h of exposure to aldosterone in a mouse inner medullary collecting duct cell line, mIMCD-3. Results from three independent microarray experiments revealed that the expression of many transcripts was affected by aldosterone treatment. Northern blot analysis confirmed the upregulation of four distinct transcripts identified by the microarray analysis, namely, the serum and glucose-regulated kinase sgk, connective tissue growth factor, period homolog, and preproendothelin. Immunoblot analysis for preproendothelin demonstrated increased protein expression. Following the levels of the four transcripts over time showed that each had a unique pattern of expression, suggesting that the cellular response to aldosterone is complex. The results presented here represent a novel list of early aldosterone-responsive transcripts and provide new avenues for elucidating the mechanism of acute aldosterone action in the kidney.

NaCl but not urea activates p38 and jun kinase in mIMCD3 murine inner medullary cells

1996 ◽  
Vol 271 (6) ◽  
pp. F1234-F1238 ◽  
Author(s):  
Z. Zhang ◽  
D. M. Cohen
Keyword(s):  
Cell Line ◽  
Collecting Duct ◽  
Renal Medulla ◽  
Duct Cell ◽  
Kinase Assay ◽  
Cellular Protection ◽  
Jun Kinase ◽  
Mitogen Activated Protein ◽  
Dose Dependent ◽  
In Cells

The mitogen-activated protein kinases (MAPKs), p38 and jun kinase (JNK), are activated by diverse stressors in cells of nonrenal medullary origin. Epithelial cells of the renal medulla are among the very few cells of higher eukaryotes routinely subjected to hyperosmotic stress, composed of principally NaCl and urea. Hyperosmotic NaCl activated p38 and JNK in a time- and dose-dependent fashion in cells of the murine terminal inner medullary collecting duct cell line (mIMCD3) as determined by immune complex kinase assay. Hyperosmotic urea exerted a minimal effect upon only p38 activation, which was evident only at 5 min. The NaCl effect was dose dependent to 800 mosmol/kgH2O; 800 mosmol/kgH2O urea, in contrast, exerted no effect. Consistent with these observations, NaCl (800 mosmol/kgH2O) but not urea (800 mosmol/kgH2O) increased tyrosine phosphorylation of p38 and JNK at 10 min. Therefore, even in the extremely osmotolerant renal medullary mIMCD3 cell line, derived from a tissue adapted for routine exposure to elevated osmolality, hypertonic NaCl activated two stress-responsive MAPKs. Urea, in contrast, exerted virtually no effect; therefore, cellular protection from urea stress operates through a mechanism distinct from the stress-responsive MAPKs.

scholarly journals FP050STUDYING MECHANISMS UNDERLYING CYSTOGENESIS IN NPHP6 IN AN EX VIVO MURINE COLLECTING DUCT CELL LINE

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii81-iii81
Author(s):  
Shalabh Srivastava ◽  
Ann Marie Hynes ◽  
Colin Miles ◽  
Rachel H Giles ◽  
John A Sayer
Keyword(s):  
Cell Line ◽  
Ex Vivo ◽  
Collecting Duct ◽  
Duct Cell

scholarly journals Transcriptome of a mouse kidney cortical collecting duct cell line: Effects of aldosterone and vasopressin

2001 ◽  
Vol 98 (5) ◽  
pp. 2712-2716 ◽  
Author(s):  
M. Robert-Nicoud ◽  
M. Flahaut ◽  
J.-M. Elalouf ◽  
M. Nicod ◽  
M. Salinas ◽  
...  
Keyword(s):  
Cell Line ◽  
Collecting Duct ◽  
Duct Cell ◽  
Mouse Kidney ◽  
Cortical Collecting Duct

Vasopressin Regulates Water Flow in a Rat Cortical Collecting Duct Cell Line Not Containing Known Aquaporins

2001 ◽  
Vol 179 (1) ◽  
pp. 63-70 ◽  
Author(s):  
C. Capurro ◽  
V. Rivarola ◽  
A. Kierbel ◽  
B. Escoubet ◽  
N. Farman ◽  
...  
Keyword(s):  
Cell Line ◽  
Water Flow ◽  
Collecting Duct ◽  
Duct Cell ◽  
Cortical Collecting Duct
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