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Molecular and Cellular Biology, February 2006, p. 1087-1097, Vol. 26, No. 3
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.3.1087-1097.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Oxidative Stress-Responsive Transcription Factor ATF3 Potentially Mediates Diabetic Angiopathy

Aki Okamoto,1,2 Yasuhiko Iwamoto,2 and Yoshiro Maru1*

Department of Pharmacology,1 Diabetes Center, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan2

Received 31 May 2005/ Returned for modification 12 July 2005/ Accepted 8 November 2005

Previous results of our cDNA microarray analysis to look for genes whose expression level correlates well with in vitro tubulogenesis by NP31 endothelial cells revealed the transcription factor ATF3 known to be responsive to stress such as reactive oxygen species (ROS). Anti-ATF3 small interfering RNA gave an inhibitory influence on tube formation by NP31 cells expressing an activated form of the vascular endothelial growth factor receptor 1 (VEGFR-1) kinase. When expression of ATF3 was regulated under the control of tetracycline system in NP31 cells, they acquired the tubulogenic ability upon ATF3 induction. While ATF3 failed to induce expressions of VEGF and VEGFR, it regulated those of CDK2, CDK4, p8, plasminogen activator inhibitor 1, integrin {alpha}1, subunit and matrix metalloprotease MMP13. In H2O2-stimulated NP31 cells as well as endothelial cells of glomerulus and aorta of Otsuka-Long-Evans-Tokushima-Fatty diabetic model rats, concomitantly enhanced expressions of ATF3, PAI-1, and p8 were observed. Given the proposed hypothesis of the close linkage between diabetic angiopathy and ROS, those data suggest that ROS-associated diabetic complication may involve ATF3-mediated pathological angiogenesis.

* Corresponding author. Mailing address: Department of Pharmacology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan. Phone and fax: 81-3-5269-7417. E-mail: ymaru{at}research.twmu.ac.jp.

Molecular and Cellular Biology, February 2006, p. 1087-1097, Vol. 26, No. 3
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.3.1087-1097.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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