| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | ADVANCED SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Biomedical Chemistry,
2 Department of Molecular and Internal Medicine and 3 Department of Clinical Laboratory Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8551, Japan
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 µm 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.
aPresent address: Division of Advanced Surgical Science and Technology, Tohoku University Graduate School of Medicine, Sendai 980–8575 Japan * Correspondence: E-mail: igarak{at}hiroshima-u.ac.jp
This article has been cited by other articles:
|
|
 |
|
  S. Mito, R. Ozono, T. Oshima, Y. Yano, Y. Watari, Y. Yamamoto, A. Brydun, K. Igarashi, and M. Yoshizumi Myocardial Protection Against Pressure Overload in Mice Lacking Bach1, a Transcriptional Repressor of Heme Oxygenase-1 Hypertension, June 1, 2008; 51(6): 1570 - 1577. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. J. Hintze, Y. Katoh, K. Igarashi, and E. C. Theil Bach1 Repression of Ferritin and Thioredoxin Reductase1 Is Heme-sensitive in Cells and in Vitro and Coordinates Expression with Heme Oxygenase1, beta-Globin, and NADP(H) Quinone (Oxido) Reductase1 J. Biol. Chem., November 23, 2007; 282(47): 34365 - 34371. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Zenke-Kawasaki, Y. Dohi, Y. Katoh, T. Ikura, M. Ikura, T. Asahara, F. Tokunaga, K. Iwai, and K. Igarashi Heme Induces Ubiquitination and Degradation of the Transcription Factor Bach1 Mol. Cell. Biol., October 1, 2007; 27(19): 6962 - 6971. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Hill-Kapturczak and A. Agarwal Haem oxygenase-1--a culprit in vascular and renal damage? Nephrol. Dial. Transplant., June 1, 2007; 22(6): 1495 - 1499. [Full Text] [PDF]
|
|
|
|
 |
|
 R. Stocker and M. A. Perrella Heme Oxygenase-1: A Novel Drug Target for Atherosclerotic Diseases? Circulation, November 14, 2006; 114(20): 2178 - 2189. [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Yano, R. Ozono, Y. Oishi, M. Kambe, M. Yoshizumi, T. Ishida, S. Omura, T. Oshima, and K. Igarashi Genetic ablation of the transcription repressor Bach1 leads to myocardial protection against ischemia/reperfusion in mice. Genes Cells, July 1, 2006; 11(7): 791 - 803. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | ADVANCED SEARCH | TABLE OF CONTENTS |
