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Primary cilia regulate gastrin secretion in GLUTag cells
Author(s) -
SaquiSalces Milena,
Merchant Juanita L.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1160.4
Subject(s) - forskolin , enteroendocrine cell , secretion , gastrin , endocrinology , medicine , chemistry , hormone , extracellular , biology , endocrine system , biochemistry , stimulation
Primary cilia (PC) are sensory organelles that we recently reported are expressed on endocrine cells of the stomach. Deletion of PC on the gastric mucosa resulted in higher plasma gastrin (Gast) levels. Therefore we hypothesized that PC on endocrine cells modulate Gast secretion. Recently we discovered that GLUTag cells present PC, in addition to expressing and releasing Gast. To define the extracellular signals regulating PC, GLUTag cells were treated with 20 mM glucose, 2% peptone, 5μM forskolin, 100 nM octreotide and 50 μM omeprazole. After 2 h tratment, PC were stained with anti‐acetylated tubulin and counted. Secreted Gast and GLP‐1 were measured and normalized to cell content. We found that glucose induced GLP‐1 but not Gast secretion and had no effect on PC. Peptone reduced PC numbers and induced Gast but not GLP‐1. Forskolin induced secretion of both hormones without affecting PC presentation. Octreotide reduced the secretion of both hormones without changing PC. However, omeprazole reduced PC numbers and increased Gast but not GLP‐1 secretion. Our data suggest that PC presentation is regulated by extracellular signals. Reduction of PC stimulated Gast secretion. PC were not associated with GLP‐1 secretion. Therefore, we concluded that GLUTag cells are a good model to study Gast release, and that PC regulate Gast but not GLP‐1 secretion. Research support: P01‐DK62041 and 5P30DK034933