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Journal of Histochemistry and Cytochemistry, Vol. 48, 123-132, January 2000, Copyright © 2000, The Histochemical Society, Inc.

ARTICLE

Apoptosis in Rat Gastric Antrum: Evidence That Regulation by Food Intake Depends on Nitric Oxide Synthase

Bao-Hong Caoa, Kirsten Mortensena, Ditte Tornehaveb, and Lars-Inge Larssona
a Division of Cell Biology, Department of Anatomy and Physiology,The Royal Veterinary and Agricultural University, Frederiksberg, Denmark
b Danish Veterinary Institute for Virus Research, Department for Pathobiology and Diagnostics, Kalvehave, Denmark

Correspondence to: Lars-Inge Larsson, Div. of Cell Biology, Dept. of Anatomy and Physiology, Royal Veterinary and Agricultural University, Gronnegaardsvej 7, DK-1870 Frederiksberg C, Denmark.

The turnover of the epithelium of the gastrointestinal tract is regulated by a balance between cell multiplication and cell loss. We examined the effects of starvation on apoptosis in endocrine and other epithelial cells of rat antropyloric mucosa. Apoptosis was determined by the TUNEL reaction combined with immunocytochemical staining for gastrin and somatostatin. Apoptotic cell morphology was determined by bisbenzimide staining for DNA. Both gastrin and somatostatin cells showed a significantly lower apoptotic index than the general epithelium. This agrees with the longer turnover kinetics of gastric endocrine cells. On starvation, the apoptotic index of the general epithelium and of the gastrin but not of the somatostatin, cells increased significantly. This was prevented by the nitric oxide synthase (NOS) inhibitor L-NAME but not by its inactive stereoisomer D-NAME. Immunoreactive neuronal NOS was present in somatostatin cells, in nonendocrine cells predominating in the surface and pit epithelium, and in rare nerve fibers. Endothelial cell NOS was present in vessels, whereas the inducible isoform was barely detectable. Thus, endogenous NOS isoforms participate in regulating antropyloric epithelial apoptosis during starvation. The close paracrine relation between somatostatin cells and gastrin cells suggests that the former regulates apoptosis of the latter through release of NO. (J Histochem Cytochem 48:123–131, 2000)

Key Words: gastrin, somatostatin, apoptosis, nitric oxide synthase, L-NAME, stomach, NO


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