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Am J Physiol Gastrointest Liver Physiol 280: G75-G87, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 1, G75-G87, January 2001

Integrin and FAK-mediated MAPK activation is required for cyclic strain mitogenic effects in Caco-2 cells

Wei Li1,2,3, Aydin Duzgun1, Bauer E. Sumpio1,2, and Marc D. Basson1,2

Departments of Surgery, 1 Yale University and 2 Connecticut Veterans Affairs Health Care System, New Haven, Connecticut 06520-8062; and 3 Tianjin Medical University Cancer Hospital, Tianjin 300060, China

Rhythmic strain stimulates Caco-2 proliferation. We asked whether mitogen-activated protein kinase (MAPK) activation mediates strain mitogenicity and characterized upstream signals regulating MAPK. Caco-2 cells were subjected to strain on collagen I-precoated membranes or antibodies to integrin subunits. Twenty-four hours of cyclic strain increased cell numbers compared with static conditions. MAPK-extracellular signal-regulated kinase (ERK) kinase inhibition (20 µM PD-98059) blocked strain mitogenicity. p38 Inhibition (10 µM SB-202190) did not. Strain rapidly and time-dependently activated focal adhesion kinase (FAK), paxillin, ERK1 and 2, and p38 on collagen. c-Jun NH2-terminal kinase (JNK)1 and 2 exhibited delayed activation. Similar activation occurred when Caco-2 cells were subjected to strain on a substrate of functional antibody to the alpha 2-, alpha 3-, alpha 6-, or beta 1-integrin subunits but not on a substrate of functional antibody to the alpha 5-subunit. FAK inhibition by FAK397 transfection blocked ERK2 and JNK1 activation by in vitro kinase assays, but pharmacological protein kinase C inhibition did not block ERK1 or 2 activation by strain. Strain-induced ERK signals mediate strain's mitogenic effects and may require integrins and FAK activation.

mitogen-activated protein kinase; deformation; epithelium; extracellular signal-regulated kinase; focal adhesion kinase; integrin; intestine; c-Jun NH2-terminal kinase; p38; signal transduction


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