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. Author manuscript; available in PMC: 2011 Feb 10.
Published in final edited form as: J Cell Physiol. 2010 Jan;222(1):230–237. doi: 10.1002/jcp.21942

Figure 1.

Figure 1

Figure 1

NO and expression of S239D-VASP in VASP-/- SMCs inhibit SMC-mediated collagen gel contraction. (A) Western blots of cell lysates of growing aortic SMCs (C57BL/6 wild-type SMCs and the following all derived from VASP-/- SMCs: LXSN SMCs, wt-VASP SMCs, S239A-VASP SMCs and S239D-VASP SMCs) were probed with antibodies against VASP or β-actin. (B) Collagen gel contraction by SMCs isolated from wild-type C57BL/6 mice or by wt-VASP SMCs was investigated in the absence or presence of a NO donor (100 μM deta NONOate). When indicated, SMCs were pretreated with deta NONOate for 30 minutes at room temperature. Data (mean±SEM; n=3-5 experiments) are expressed as percent of gel contraction. * With vs. without deta NONOate, P ≤ 0.05. (C) Collagen gel contraction by LXSN, wt-VASP, S239A-VASP or S239D-VASP SMCs. Data (mean±SEM; n=3-5 experiments) are expressed as the percent of gel contraction. * S239D-VASP SMCs vs. other cell types, P ≤ 0.05. (D) Collagen gel contraction by LXSN, wt-VASP, S239A-VASP or S239D-VASP SMCs in absence or presence of deta NONOate. Data (mean±SEM; n=3-5 experiments) are expressed as percent of gel contraction. * With vs. without deta NONOate, P ≤ 0.05.