Journal
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 278, Issue 1, Pages C212-C233Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.2000.278.1.C212
Keywords
adenosine; cholinergic; histamine; inflammatory bowel disease; prostaglandin E-2
Categories
Funding
- NIDDK NIH HHS [DK-39007] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R55DK039007, R01DK039007, R29DK039007] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Crypts of Lieberkuhn were isolated from human colon, and differential interference contrast microscopy distinguished goblet and columnar cells. Activation with carbachol (CCh, 100 mu M) or histamine (10 mu M) released contents from goblet granules. Stimulation with prostaglandin E-2 (PGE(2), 5 mu M) or adenosine (10 mu M) did not release goblet granules but caused the apical margin of columnar cells to recede. Goblet volume was lost during stimulation with CCh or histamine (similar to 160 fl/cell), but not with PGE(2) or adenosine. Three-quarters of goblet cells were responsive to CCh but released only 30% of goblet volume. Half-time for goblet volume release was 3.7 min. PGE(2) stimulated a prolonged fluid secretion that attained a rate of similar to 350 pl/min. Columnar cells lost similar to 50% of apical volume during maximal PGE(2) stimulation, with a half-time of 3.3 min. In crypts from individuals with ulcerative colitis, goblet cells were hypersensitive to CCh for release of goblet volume. These results support separate regulation for mucus secretions from goblet cells and from columnar cells, with control mechanisms restricting total release of mucus stores.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Recommended
No Data Available