Secretory Control of Basolateral Membrane Potassium and Chloride Channels in Colonic Crypt Cells

Author(s):  
Dan R. Halm
1997 ◽  
Vol 272 (4) ◽  
pp. G732-G741 ◽  
Author(s):  
U. Sundaram ◽  
A. B. West

The effect of chronic inflammation on electrolyte transport in rabbit ileal villus and crypt cells was determined with the use of a rabbit model of chronic ileitis. In both cells, Na+/H+ exchange was monitored by following recovery from an acid load, and Cl-/HCO3- exchange was monitored by following recovery from an alkaline load. In villus cells, recovery from an acid load was not affected; however, recovery from an alkaline load was slowed. These data suggest that chronic inflammation inhibits Cl-/HCO3- exchange in villus cells. In contrast, in crypt cells, recovery from an alkaline load was unaffected, whereas recovery from an acid load was accelerated. These data suggest that chronic inflammation stimulates Na+/H+ exchange in crypt cells. Inhibition of Cl-/HCO3- exchange in villus cells would be expected to inhibit coupled NaCl absorption, which occurs by the coupling of brush-border membrane (BBM) Na+/H+ and Cl-/HCO3- exchange. Stimulation of Na+/H+ exchange in crypt cells, known to be present only on the basolateral membrane, alkalinizes the cell. This alkalinization may stimulate BBM Cl-/HCO3- exchange, resulting in HCO3- secretion. Thus these unique alterations in transporter activity suggest that different endogenous immune-inflammatory mediators may have differing effects on specific transporters in villus and crypt cells in the chronically inflamed ileum.


1998 ◽  
Vol 275 (1) ◽  
pp. E124-E131 ◽  
Author(s):  
Karen E. Sheppard ◽  
Karen Khoo ◽  
Zygmunt S. Krozowski ◽  
Kevin X. Z. Li

Recently, we identified a novel putative nuclear receptor in colonic crypt cells distinct from both mineralocorticoid receptor and glucocorticoid receptor, with high affinity for 11-dehydrocorticosterone (11-DHB) (33). In the present study, competitive nuclear binding assays demonstrated that this site has a unique steroid binding specificity that distinguishes it from other steroid receptors. Western blot analysis showed the presence of 11β-hydroxysteroid dehydrogenase-2 (11βHSD2) but not 11βHSD1 in colonic crypt cells and showed that 11βHSD2 was present in the nuclear pellet. Differences in steroid specificity between the putative DHB receptor and inhibition of 11βHSD activity indicate that binding is not to the enzyme. Furthermore, modified Chinese hamster ovary cells transfected with the 11βHSD2 gene express nuclear 11βHSD2 but not a nuclear DHB binding site. In conclusion, these data support the existence of a novel nuclear DHB receptor in rat colon that is distinct from the classic steroid receptors and from both 11βHSD1 and 11βHSD2.


1987 ◽  
Vol 252 (2) ◽  
pp. G170-G177 ◽  
Author(s):  
J. R. Walters ◽  
M. M. Weiser

Rat duodenal cells were isolated sequentially to give fractions enriched for villus and crypt cells. From each of these fractions, basolateral-enriched membrane vesicles were prepared and ATP-dependent calcium uptake was studied. Calcium uptake was sensitive to temperature, was inhibited by vanadate and by A23187, and was lower in vitamin D-deficient animals. In normal animals, calcium transport was approximately twofold greater in villus-tip than in crypt cell-fraction basolateral membranes though the affinity of the uptake for calcium was similar (Km = 0.3 microM). In vitamin D-deficient animals, the crypt-to-villus gradient was reduced, and in all fractions, calcium transport was similar to or lower than that in the crypts of normal animals. Six hours after vitamin D-deficient animals were repleted with 1,25-dihydroxycholecalciferol, a significant increase in calcium transport by everted gut sacs was present; however, basolateral calcium transport was significantly increased in only the mid-villus fractions, and no change was seen in the villus-tip fractions. Thus vitamin D appears necessary for the development of increased basolateral membrane calcium pump activity in duodenal villus cells, but not all cells in vitamin D-deficient rats are able to respond to 1,25-dihydroxycholecalciferol.


1989 ◽  
Vol 26 (3) ◽  
pp. 280-280
Author(s):  
S Walther ◽  
P Heinz-Erian ◽  
A Roscher ◽  
Y Shin-Zoulek ◽  
W Stolz ◽  
...  

1997 ◽  
Vol 435 (2) ◽  
pp. 267-272 ◽  
Author(s):  
M. S. Nielsen ◽  
R. Warth ◽  
M. Bleich ◽  
B. Weyand ◽  
R. Greger

1996 ◽  
Vol 432 (6) ◽  
pp. 1011-1022 ◽  
Author(s):  
M. Bleich ◽  
N. Riedemann ◽  
R. Warth ◽  
D. Kerstan ◽  
J. Leipziger ◽  
...  

2011 ◽  
Vol 17 ◽  
pp. S72
Author(s):  
Joel Pekow ◽  
Maria Westerhoff ◽  
John Hart ◽  
Marc Bissonnette
Keyword(s):  

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