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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00056.2002
Submitted on February 11, 2002
Accepted on March 18, 2002
1 Department of Physiology, University of Liverpool, Liverpool, United Kingdom
* To whom correspondence should be addressed. E-mail: avarro{at}liverpool.ac.uk.
Epithelial organisation is maintained by cell proliferation, migration and differentiation. In the case of the gastric epithelium, at least some of these events are regulated by the hormone gastrin. In addition, gastric epithelial cells are organised into characteristic tubular structures (the gastric glands), but the cellular mechanisms regulating the organisation of tubular structures (sometimes called branching morphogenesis) are uncertain. In the present study we examined the role of the gastrin-cholecystokinin(CCK)B receptor in promoting branching morphogenesis of gastric epithelial cells. When gastric cancer AGS-GR cells were cultured on plastic, gastrin and phorbol ester (PMA) stimulated cell adhesion, formation of lamellipodia and extension of long processes in part by activation of protein kinase C, and phosphatidylinositol(PI)-3-kinase. Branching morphogenesis was not observed in these circumstances. However, when cells were cultured on artificial basement membrane the same stimuli increased the formation of organised multicellular arrays, exhibiting branching morphogenesis. These effects were reversed by inhibitors of protein kinase C, but not PI-3-kinase. We conclude that in the presence of basement membrane, activation of protein kinase C (PKC) by gastrin stimulates branching morphogenesis.
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