Instead, expression of vimentin (Fig. 2, A and B) and fibronectin (Fig. 2, A and C) was highly upregulated in the injured region, suggesting that the laser injury resulted in an activation of fibroblasts, which then deposited a fibronectin-rich ECM that is reminiscent of replacement fibrosis found post-MI in vivo. This evidence concerns the gene VIM and myocardial infarction.