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Endocrinology Vol. 139, No. 10 4380-4390
Copyright © 1998 by The Endocrine Society

ARTICLES

Growth Factor Effects on Apoptosis of Rat Gastric Enterochromaffin-Like Cells1

Sabine Mahr, Nina Neumayer, Helmut J. Kolb, Wolfgang Schepp, Meinhard Classen and Christian Prinz

Department of Medicine II, Technical University of Munich (S.M., N.N., W.S., M.C., C.P.), and the Department of Clinical Chemistry, Harlaching Municipal Hospital (H.J.K.), D-81675 Munich, Germany

Address all correspondence and requests for reprints to: Christian Prinz, M.D., Second Department of Medicine, Technical University of Munich, Ismaninger Strasse 22, D-81675 Munich, Germany. E-mail: christian.prinz{at}lrz.tum.de

Enterochromaffin-like (ECL) cells are histamine-containing endocrine cells in the gastric epithelium that show increased density during chronic atrophic gastritis. The current study determined cell number and apoptosis of isolated rat ECL cells in response to several growth factors. Isolated ECL cells from fundic mucosa (enrichment >90%) were grown in serum-free medium over 2–5 days. Cell number was determined by mitochondrial formazan production; apoptosis was measured by Tdt-mediated dUTP nick end labeling reaction and DNA fragmentation-based enzyme-linked immunosorbent assay. Immunocytochemistry and RT-PCR demonstrated the presence of epidermal growth factor receptor, neuronal growth factor receptor (type 1), and fibroblast growth factor (FGF) receptor (type 1). Gastrin (EC50, ~2 pM), transforming growth factor-{alpha} (TGF{alpha}; 10–30 ng/ml), and basic FGF (bFGF; 1–10 ng/ml) increased the total number of cultured ECL cells. bFGF augmented the gastrin (1 pM)-induced response. ß-Neuronal growth factor (10 ng/ml) and bFGF (2 ng/ml) decreased the programed death of ECL cells. Interleukin-1ß (100 pg/ml, 24 h) stimulated apoptosis 2- to 3-fold in ECL cells, and simultaneous incubation with TGF{alpha} (20 ng/ml) or bFGF (2 ng/ml) significantly inhibited this effect. ECL cells express specific receptors for gastrin, epidermal growth factor, neuronal growth factor, and FGF. bFGF prolonged ECL cell survival by inhibiting spontaneous apoptosis. Our data further indicate that TGF{alpha} and bFGF increase ECL cell number by inhibiting cytokine-induced programed cell death.




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