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Carbachol-induced colonic mucus formation requires transport via NKCC1, K(+) channels and CFTR.

Artikel i vetenskaplig tidskrift
Författare Jenny K Gustafsson
Sara K. Lindén
Ala H Alwan
Bob J Scholte
Gunnar C. Hansson
Henrik Sjövall
Publicerad i Pflugers Archiv : European journal of physiology
Volym 467
Nummer/häfte 7
Sidor 1403-1415
ISSN 1432-2013
Publiceringsår 2015
Publicerad vid Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 1403-1415
Språk en
Länkar dx.doi.org/10.1007/s00424-014-1595-...
Ämnesord mucus, charbachol, mucus formation, ion transport
Ämneskategorier Cellbiologi

Sammanfattning

The colonic mucosa protects itself from the luminal content by secreting mucus that keeps the bacteria at a distance from the epithelium. For this barrier to be effective, the mucus has to be constantly replenished which involves exocytosis and expansion of the secreted mucins. Mechanisms involved in regulation of mucus exocytosis and expansion are poorly understood, and the aim of this study was to investigate whether epithelial anion secretion regulates mucus formation in the colon. The muscarinic agonist carbachol was used to induce parallel secretion of anions and mucus, and by using established inhibitors of ion transport, we studied how inhibition of epithelial transport affected mucus formation in mouse colon. Anion secretion and mucin exocytosis were measured by changes in membrane current and epithelial capacitance, respectively. Mucus thickness measurements were used to determine the carbachol effect on mucus growth. The results showed that the carbachol-induced increase in membrane current was dependent on NKCC1 co-transport, basolateral K(+) channels and Cftr activity. In contrast, the carbachol-induced increase in capacitance was partially dependent on NKCC1 and K(+) channel activity, but did not require Cftr activity. Carbachol also induced an increase in mucus thickness that was inhibited by the NKCC1 blocker bumetanide. However, mice that lacked a functional Cftr channel did not respond to carbachol with an increase in mucus thickness, suggesting that carbachol-induced mucin expansion requires Cftr channel activity. In conclusion, these findings suggest that colonic epithelial transport regulates mucus formation by affecting both exocytosis and expansion of the mucin molecules.

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