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Pass the bicarb: the importance of HCO3– for mucin release
Robert C. De Lisle
Robert C. De Lisle
Published August 24, 2009
Citation Information: J Clin Invest. 2009;119(9):2535-2537. https://doi.org/10.1172/JCI40598.
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Pass the bicarb: the importance of HCO3– for mucin release

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Abstract

Accumulation of thick, sticky mucus is a hallmark of the genetic disease cystic fibrosis (CF) and has a central role in CF pathophysiology. Mutations in the CF transmembrane regulator (CFTR) ion channel are known to result in abnormally thick and sticky mucus; however, why mucus accumulates in CF is still not completely understood. In this issue of the JCI, Garcia and colleagues show that mucin — the heavily glycosylated protein contained within mucus — requires CFTR and bicarbonate in order to be released from mouse intestine (see the related article beginning on page 2613). The authors propose a model whereby CFTR-mediated bicarbonate secretion must be concurrent with mucin exocytosis for proper mucin release.

Authors

Robert C. De Lisle

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Figure 2

Schematic model summarizing potential sites of action of CFTR and HCO3– in mucin release.

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Schematic model summarizing potential sites of action of CFTR and HCO3– ...
HCO3– is taken up from the serosal space and transported into the gut lumen in a CFTR-dependent manner by the enterocyte. CFTR acts as an HCO3– channel to directly transport HCO3– and also acts indirectly by supplying Cl– to the lumen, which is then exchanged for HCO3– (arrow) by Cl–/HCO3– exchangers. The study in this issue by Garcia et al. (6) reports that HCO3– and CFTR are required for mucin secretion. The authors propose that, upon mucin secretion from goblets cells into the lumen, the mucins (previously condensed into mucin granules) rapidly disassociate from Ca2+ and H+ ions, which allows mucin expansion and disaggregation and the formation of a normal mucus layer. However, Garcia et al. also report that direct addition of HCO3– to the gut lumen is insufficient to support mucin release. This suggests the possibility that HCO3– does not act at the luminal surface in mucin release. Are there intracellular functions of HCO3– and CFTR, such as fostering intercellular communication between the enterocyte and the goblet cell (e.g., intracellular pH regulation and gap junction communication), that potentiate mucin granule exocytosis?

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ISSN: 0021-9738 (print), 1558-8238 (online)

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