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Non-CFTR chloride channels likely contribute to secretion in the murine small intestine.
Pflugers Arch 2001; 443 Suppl 1:S103-6PA

Abstract

While most cystic fibrosis (CF) transmembrane conductance regulator (CFTR)-knockout animals die due to intestinal obstruction before or at the time of weaning, a subpopulation of these animals are long living and exhibit a milder phenotype. The decreased severity of intestinal disease in these mildly affected CF mice is related to the expression of non-CFTR genetic modifiers. The identity of these genetic modifiers is not known, but we hypothesize that they may complement CFTR function as a chloride channel in this tissue. To assess the contribution of non-CFTR chloride channels to chloride secretion across the small intestine of CF mice with mild disease, we measured the basal transepithelial potential difference across this tissue as well as the secretory response to agonists of the cAMP and the calcium-mediated signaling pathways. Chloride secretion across the small intestine of mildly affected CF mice was not stimulated by forskolin or by carbachol. The absence of CFTR is thus not compensated by the activity of a distinct, cAMP- or calcium-activated chloride channel at the apical surface of the intestinal epithelium. On the other hand, a basal chloride secretion across the intestinal epithelium was present in these animals, and we hypothesize that this activity may be linked to improved survival of these animals.

Authors+Show Affiliations

Department of Structural Biology and Biochemistry, The Hospital for Sick Children, 55 University Ave., Toronto, M5G 1X8, Ontario, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11845313

Citation

Gyömörey, K, et al. "Non-CFTR Chloride Channels Likely Contribute to Secretion in the Murine Small Intestine." Pflugers Archiv : European Journal of Physiology, vol. 443 Suppl 1, 2001, pp. S103-6.
Gyömörey K, Garami E, Galley K, et al. Non-CFTR chloride channels likely contribute to secretion in the murine small intestine. Pflugers Arch. 2001;443 Suppl 1:S103-6.
Gyömörey, K., Garami, E., Galley, K., Rommens, J. M., & Bear, C. E. (2001). Non-CFTR chloride channels likely contribute to secretion in the murine small intestine. Pflugers Archiv : European Journal of Physiology, 443 Suppl 1, pp. S103-6.
Gyömörey K, et al. Non-CFTR Chloride Channels Likely Contribute to Secretion in the Murine Small Intestine. Pflugers Arch. 2001;443 Suppl 1:S103-6. PubMed PMID: 11845313.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Non-CFTR chloride channels likely contribute to secretion in the murine small intestine. AU - Gyömörey,K, AU - Garami,E, AU - Galley,K, AU - Rommens,J M, AU - Bear,C E, Y1 - 2001/07/06/ PY - 2002/2/15/pubmed PY - 2002/5/8/medline PY - 2002/2/15/entrez SP - S103 EP - 6 JF - Pflugers Archiv : European journal of physiology JO - Pflugers Arch. VL - 443 Suppl 1 N2 - While most cystic fibrosis (CF) transmembrane conductance regulator (CFTR)-knockout animals die due to intestinal obstruction before or at the time of weaning, a subpopulation of these animals are long living and exhibit a milder phenotype. The decreased severity of intestinal disease in these mildly affected CF mice is related to the expression of non-CFTR genetic modifiers. The identity of these genetic modifiers is not known, but we hypothesize that they may complement CFTR function as a chloride channel in this tissue. To assess the contribution of non-CFTR chloride channels to chloride secretion across the small intestine of CF mice with mild disease, we measured the basal transepithelial potential difference across this tissue as well as the secretory response to agonists of the cAMP and the calcium-mediated signaling pathways. Chloride secretion across the small intestine of mildly affected CF mice was not stimulated by forskolin or by carbachol. The absence of CFTR is thus not compensated by the activity of a distinct, cAMP- or calcium-activated chloride channel at the apical surface of the intestinal epithelium. On the other hand, a basal chloride secretion across the intestinal epithelium was present in these animals, and we hypothesize that this activity may be linked to improved survival of these animals. SN - 0031-6768 UR - https://www.unboundmedicine.com/medline/citation/11845313/Non_CFTR_chloride_channels_likely_contribute_to_secretion_in_the_murine_small_intestine_ L2 - https://dx.doi.org/10.1007/s004240100654 DB - PRIME DP - Unbound Medicine ER -