Fig. 1
From: Vimentin dephosphorylation at ser-56 is regulated by type 1 protein phosphatase in smooth muscle
Inhibition of protein phosphatases 1 and 2A induces contraction and vimentin phosphorylation at Ser-56 in airway smooth muscle. a Upper panel: A representative force tracing illustrating the effects of okadaic acid (OA), a potent inhibitor of protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A) on mouse tracheal rings. Lower panel: A representative force tracing showing the effects of okadaic acid on the precontracted mouse tracheal rings. b Mouse tracheal rings were treated with different concentrations of okadaic acid. Contraction in these tissues was then evaluated. Tracheal contraction is normalized to the maximal contraction induced by okadaic acid. Data represent mean ± SE (n = 5). **, p < 0.01 vs. untreated tissues. c Mouse tracheal rings were treated with 10−6M okadaic acid for 1 – 10 min. Vimentin phosphorylation at Ser-56 in tissues was evaluated by immunoblot analysis. OA-induced vimentin phosphorylation is normalized to the value of untreated tissues. Vimentin phosphorylation is significantly higher in rings treated with okadaic acid than in untreated rings (*, p < 0.05). Data represent mean ± SE (n = 7–11). d Contraction is normalized to the maximal contraction induced by okadaic acid (10−6 M, 10 min). Data represent mean ± SE (n = 7–11). *, p < 0.05 vs. untreated tissues