Cystic fibrosis transmembrane conductance regulator and Na<sup>+</sup> channel subunits mRNA transcripts, and Cl<sup>−</sup> efflux, show a different distribution in rat duodenum and colon

Odes, H S; Smirnoff, Patricia; Guberman, R; Pollak-Charcon, Sylvie; Sperber, Ami D.; Fich, Alexander; Fraser, Gerald; Schwartz, Betty

doi:10.1046/j.1365-201x.2003.01138.x

Cited by 9 publications

(6 citation statements)

References 41 publications

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“…basolateral membranes of crypts and its abundance decreased toward the villus tip, but it was clearly detected on the basolateral membranes of villus enterocytes, supporting the observations by others that villus cells participate in anion secretion (23,27,32).…”

Section: Resultssupporting

confidence: 75%

STa and cGMP stimulate CFTR translocation to the surface of villus enterocytes in rat jejunum and is regulated by protein kinase G

Golin-Bisello¹,

Bradbury²,

Ameen³

2005

American Journal of Physiology-Cell Physiology

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Section: Resultssupporting

confidence: 75%

STa and cGMP stimulate CFTR translocation to the surface of villus enterocytes in rat jejunum and is regulated by protein kinase G

Golin-Bisello¹,

Bradbury²,

Ameen³

2005

American Journal of Physiology-Cell Physiology

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“…CFTR was undetectable in CFTR -/-tissue ( Figure 2C). In wild-type ileum, CFTR localized to the apical membrane of crypt, but not villous epithelia, consistent with other reports of endogenous CFTR localization in the intestine (14,(24)(25)(26). In line e, we detected CFTR variably present at the apical membrane of crypt epithelial cells.…”

Section: Introductionsupporting

confidence: 79%

Intestinal CFTR expression alleviates meconium ileus in cystic fibrosis pigs

Stoltz¹,

Rokhlina²,

Ernst³

et al. 2013

J. Clin. Invest.

115

127

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Cystic fibrosis (CF) pigs develop disease with features remarkably similar to those in people with CF, including exocrine pancreatic destruction, focal biliary cirrhosis, micro-gallbladder, vas deferens loss, airway disease, and meconium ileus. Whereas meconium ileus occurs in 15% of babies with CF, the penetrance is 100% in newborn CF pigs. We hypothesized that transgenic expression of porcine CF transmembrane conductance regulator (pCFTR) cDNA under control of the intestinal fatty acid-binding protein (iFABP) promoter would alleviate the meconium ileus. We produced 5 CFTR -/-;TgFABP>pCFTR lines. In 3 lines, intestinal expression of CFTR at least partially restored CFTR-mediated anion transport and improved the intestinal phenotype. In contrast, these pigs still had pancreatic destruction, liver disease, and reduced weight gain, and within weeks of birth, they developed sinus and lung disease, the severity of which varied over time. These data indicate that expressing CFTR in intestine without pancreatic or hepatic correction is sufficient to rescue meconium ileus. Comparing CFTR expression in different lines revealed that approximately 20% of wild-type CFTR mRNA largely prevented meconium ileus. This model may be of value for understanding CF pathophysiology and testing new preventions and therapies.

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“…However, it should be noted that NHE inhibition increases rather than decreases DMBS (Repishti et al 2001, Furukawa et al 2004, therefore the decrease in acid-induced DMBS is most likely due to the inhibitive effect of amiloride on ASICs. Although ENaC is an important pathway for Na + entry into a variety of epithelial cells, its b-subunit expression is lacking in the duodenal epithelium, making duodenal ENaC inactive (Odes et al 2003). Our data showing molecular and functional expression of ASIC1a in intestinal epithelial cells have provided further supports for its involvement in mediating acid-stimulated DMBS.…”

supporting

confidence: 59%

“…There exists the possibility that our results could be caused by the inhibition of NHE by amiloride; however, it should be noted that the inhibition of the NHE actually activates DMBS 22, 23 , therefore the decrease in DMBS must be caused by the inhibitive effect of amiloride on ASICs. Although it is an important pathway for Na + entry into a variety of epithelial cells, expression of ENaC β-subunit is lacking in the duodenal epithelium, making the activity of duodenal ENaC unlikely 24 . Taken together, our data showing both expression and function of ASIC1a in intestinal epithelial cells have provided support for its important role in mediating acid-stimulated DMBS.…”

Section: Discussionmentioning

confidence: 99%

Expression of acid‐sensing ion channels in intestinal epithelial cells and their role in the regulation of duodenal mucosal bicarbonate secretion

Dong

Chow

et al. 2010

Acta Physiologica

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Although acid-sensing ion channels (ASICs) have been studied in a variety of mammalian cells, little is currently known about their presence in intestinal epithelial cells. Therefore, the aims of the present study were to investigate the expression and function of ASIC isoforms in intestinal epithelial cells, particularly their physiological role in the acid-stimulated duodenal mucosal bicarbonate secretion (DMBS). RT-PCR and digital Ca2+ imaging were used to determine the expression and function of ASICs in HT29 cells, a human intestinal epithelial cell line. The acid-stimulated DMBS was measured in C57 black mice in vivo to study the role of ASICs in this physiological process. mRNA expression of ASIC1a was detected in the duodenal mucosa stripped from mice and HT29 cells, in which cytoplasmic free Ca2+ ([Ca2+]cyt) in response to extracellular acidosis was also measured. In Ca2+-containing solutions, acidosis raised [Ca2+]cyt in a pH-dependent manner with a half-maximal effect (pH0.5) at approximately 5.9. The acidosis-induced increase in [Ca2+]cyt was markedly inhibited by amiloride (an ASIC blocker), SK&F96365 (a blocker for non-selective cation channels), or in Ca2+-free solutions; but slightly affected by U73122, or nifedipine. After acidosis raised [Ca2+]cyt, stimulation of purinergic receptors with ATP further increased [Ca2+]cyt. Moreover, the acid-stimulated murine DMBS was significantly attenuated by amiloride. Therefore, ASIC1a is functionally expressed in intestinal epithelial cells, and may play an important role in the regulation of [Ca2+]cyt homeostasis in these cells and the acid-stimulated DMBS.

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Cystic fibrosis transmembrane conductance regulator and Na⁺ channel subunits mRNA transcripts, and Cl⁻ efflux, show a different distribution in rat duodenum and colon

Cited by 9 publications

References 41 publications

STa and cGMP stimulate CFTR translocation to the surface of villus enterocytes in rat jejunum and is regulated by protein kinase G

STa and cGMP stimulate CFTR translocation to the surface of villus enterocytes in rat jejunum and is regulated by protein kinase G

Intestinal CFTR expression alleviates meconium ileus in cystic fibrosis pigs

Expression of acid‐sensing ion channels in intestinal epithelial cells and their role in the regulation of duodenal mucosal bicarbonate secretion

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Cystic fibrosis transmembrane conductance regulator and Na+ channel subunits mRNA transcripts, and Cl− efflux, show a different distribution in rat duodenum and colon

Cited by 9 publications

References 41 publications

STa and cGMP stimulate CFTR translocation to the surface of villus enterocytes in rat jejunum and is regulated by protein kinase G

STa and cGMP stimulate CFTR translocation to the surface of villus enterocytes in rat jejunum and is regulated by protein kinase G

Intestinal CFTR expression alleviates meconium ileus in cystic fibrosis pigs

Expression of acid‐sensing ion channels in intestinal epithelial cells and their role in the regulation of duodenal mucosal bicarbonate secretion

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Cystic fibrosis transmembrane conductance regulator and Na⁺ channel subunits mRNA transcripts, and Cl⁻ efflux, show a different distribution in rat duodenum and colon