Bach1 is a transcriptional repressor of the cytoprotective enzyme heme 
oxygenase-1 (HO-1). Although HO-1 protects against atherosclerosis, the function 
of Bach1 in this process is poorly understood. We isolated peritoneal 
macrophages and aortic smooth muscle cells (SMC) from wild-type and 
bach1-deficient mice. bach1-Deficient macrophages expressed increased levels of 
HO-1 and showed elevated phagocytic activity when incubated with 0.75 microm 
microspheres. In SMC, bach1-ablation resulted in increased expression of HO-1 
and decreased proliferation in bromodeoxyuridine incorporation assay as compared 
with wild-type cells. The up-regulated phagocytic activity and reduced SMC 
proliferation of bach1-deficient cells were not restored by Zinc (II) 
protoporphyrin IX, an inhibitor of HO, suggesting that HO-independent mechanisms 
are also involved in the regulation of phagocytosis of macrophages and 
proliferation of SMC by Bach1. In wild-type mice, cuff placement around femoral 
artery caused pronounced intimal proliferation without affecting the media, thus 
resulting in intimal to medial (I/M) volume ratio of 65.6%. bach1-deficient mice 
had less degree of intimal growth (I/M ratio of 45.6%). These results indicate 
that Bach1 plays a critical role in the regulation of HO-1 expression, 
macrophage function, SMC proliferation and neointimal formation. Bach1 may 
regulate gene expression in these cells during inflammation and atherogenesis.