Mechanisms of Lectin (Phytohemagglutinin)-Induced Growth in Small Intestinal Epithelial Cells (original) (raw)

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Research Articles| December 21 2001

Jan-Michel Otte;

1st Department of Internal Medicine, Christian Albrecht University, Kiel, Germany

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Chunxiao Chen;

1st Department of Internal Medicine, Christian Albrecht University, Kiel, Germany

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Gabriele Brunke;

1st Department of Internal Medicine, Christian Albrecht University, Kiel, Germany

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Karlheinz Kiehne;

1st Department of Internal Medicine, Christian Albrecht University, Kiel, Germany

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Frank Schmitz;

1st Department of Internal Medicine, Christian Albrecht University, Kiel, Germany

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Ulrich R. Fölsch;

1st Department of Internal Medicine, Christian Albrecht University, Kiel, Germany

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Karl-Heinz Herzig

1st Department of Internal Medicine, Christian Albrecht University, Kiel, Germany

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Digestion (2001) 64 (3): 169–178.

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Abstract

Background/Aims: The lectin phytohemagglutinin is a mitogen for intestinal epithelial cells in vivo. The mechanisms of action are unknown and were therefore analyzed in vitro. Methods: Human (Intestine-407) and rat (IEC-6; IEC-18) intestinal epithelial cell lines were stimulated with phytohemagglutinin. Proliferation was assayed by 3H-thymidine incorporation, activation of mitogen-activated protein kinase (MAPK) by Western blotting, and induction of c-fos mRNA expression by semiquantitative polymerase chain reaction. Control experiments were performed with phenyl-N-acetyl-α-_D_-galactosaminide or the tyrosine kinase inhibitor tyrphostin A25. Results: Phytohemagglutinin (0.1 µg/ml) significantly stimulated proliferation in all three cell lines after 48–72 h. MAPK activation was detected after 15–30 min, and an induction of c-fos mRNA expression after 15– 30 min of stimulation. Mitogenic effects were blocked by preincubation with phenyl-N-acetyl-α-_D_-galactosaminide or tyrphostin A25. Conclusion: Phytohemagglutinin stimulated proliferation, MAPK activation and induction of c-fos mRNA expression. The lectin may contribute to intestinal mucosal growth and regeneration thereby preventing gut atrophy.

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© 2001 S. Karger AG, Basel

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