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. 2008 Jul 10;118(8):2733–2746. doi: 10.1172/JCI32381

Figure 10. Ang II–induced migration via the LR11/uPAR pathway in SMCs.

Figure 10

(A) Effect of blocking LR11 activation on the Ang II–induced increase of attachment of rabbit SMCs. The SMCs attached to plastic plates were counted after incubation in the presence or absence of Ang II (1 μM) with or without valsartan (10 nM), anti-LR11 antibody, or sLR11 (1 μg/μl). Data are presented as mean ± SD (n = 3). *P < 0.05. (B) Effect of uPAR silencing on the Ang II–induced increase in rabbit SMCs migration. The migrated SMCs treated with exogeneous siRNA specific for uPAR or control (Cont.) RNA were counted after incubation in the presence or absence of Ang II (1 μM) with or without candesartan (10 nM). Inset: Membrane extracts (10 μg protein) prepared from these cells were subjected to immunoblot analysis with anti-uPAR (~50 kDa) or anti-LR11 antibody (~250 kDa). Data are presented as mean ± SD (n = 3). (C) Effect of Ang II on the PDGF-induced migration of LR11-overexpressing SMCs. The number of migrated A7r5 cells transfected with LR11 cDNA (R-1), or control cells (C-1) in the presence or absence of PDGF-BB (PDGF, 10 ng/ml) were determined after incubation with or without sLR11 (1 μg/μl), Ang II (1 μM), or valsartan (10 nM). Data are presented as mean ± SD (n = 10).