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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 
2-,
3-, 6-, or 
1-integrin subunits but not on a substrate of
functional antibody to the 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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