Fig. 2.

Signal interaction in response to strain. Downstream signals were studied in Caco-2 cells under static (open bars) and cyclic strain (solid bars) conditions during upstream signal inhibition. A: blocking PI3K blocks strain-induced extracellular signal-related kinase (ERK) activation. Blocking AKT does not (n = 10, *P < 0.05, **P < 0.01). B: similarly, PI3K inhibition prevents strain-induced p38 activation, whereas AKT inhibition does not (n ≥ 8, *P < 0.05, **P < 0.01). Furthermore, strain-induced GSK phosphorylation was blocked by PI3K inhibition (C, n = 9, *P < 0.01), AKT inhibition (D, n = 8, *P < 0.0001), and ERK inhibition (E, n = 10, *P < 0.0001). F: p38 inhibition did not block GSK phosphorylation (n = 6, *P < 0.001).