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. 2011 Mar 10;6(3):e17771. doi: 10.1371/journal.pone.0017771

Figure 5. Evaluation of the role of Rho A/Rho kinase- and Ca2+/CaM/MLCK-dependent pathways in the contraction of SMPCs and hVSMCs.

Figure 5

CD34+PDGF or CD34+RA cells were initially treated for 3 days with serum-free medium containing the agonists endothelin-1 (End-1 (10 nM), A and B.1) or U46619 (1 µM) (A and B.2) in the presence or absence of the Rho-kinase inhibitor Y27632 (13 µM) or the calmodulin inhibitor W-7 (12 µg/mL). The cells were then encapsulated in fibrin gels and the diameter of the gel assessed at time 0 (1) and 14 h (2,3,4). Graph displays the variation in gel diameter (percentage) encapsulating hVSMCs (2), CD34+PDGFBB cells (3) or CD34+RA cells (4). Data are shown as mean ± SEM (n = 6), * P<0.001 relatively to samples inhibited with Y27632 or W-7, by Student's t-test.