The regulation of vascular smooth muscle cell proliferation by beta-catenin signalling in vivo

Cell-cell adhesion is critical in the maintenance of normal cellular functions. De-regulated cell-cell adhesion and consequent cell signalling in vascular smooth muscle cells (VSMCs) may contribute to the development of intimal thickening that leads to blockage of blood vessels and heart disease, a major clinical problem. In this project, we tested two main hypotheses:
a) that beta-catenin signalling contributes to VSMC proliferation by the up-regulation of cyclin D1 and down-regulation of p21 and therefore contributes to intimal thickening in restenosis and atherosclerosis.
b) that beta-catenin signalling is regulated by a combination of N-cadherin levels and the Wnt pathway in VSMCs.

Wnt4 was identified as the key Wnt involved VSMC proliferation during mouse intimal thickening