Proposed models for BMP regulation of hPASMC motility and proliferation by recruitment of Wnt–βC and Wnt–PCP signaling. (A) BMP-2 triggers βC accumulation via pAkt-mediated GSK3β inhibition followed by production and release of FN to the extracellular space (1). By binding to α4β1-integrin, FN activates ILK-1 and induces formation of a complex between ILK-1 and Dvl leading to RhoA and Rac1 activation (2) and simultaneous suppression of βC activation (3). (B) The inability to form or maintain a complex between ILK-1 and Dvl may facilitate hPASMC proliferation in response to growth factors such as PDGF-BB by enhancing βC signaling through ILK-1–mediated GSK3β inhibition. APC, adenomatous polyposis coli.