Both authors contributed equally.
Proteomic profiling and identification of cofilin responding to oxidative stress in vascular smooth muscle
Article first published online: 10 NOV 2006
Copyright © 2006 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Volume 6, Issue 24, pages 6455–6475, No. 24 December 2006
How to Cite
Lee, C.-K., Park, H.-J., So, H. H., Kim, H. J., Lee, K. S., Choi, W. S., Lee, H. M., Won, K.-J., Yoon, T. J., Park, T.-K. and Kim, B. (2006), Proteomic profiling and identification of cofilin responding to oxidative stress in vascular smooth muscle. Proteomics, 6: 6455–6475. doi: 10.1002/pmic.200600124
- Issue published online: 12 DEC 2006
- Article first published online: 10 NOV 2006
- Manuscript Received: 18 FEB 2006
- Korea Research Foundation Grant funded by the Korean Government (MOEHERD, KRF-2005-015-E00021)
- Regional Research Centers Program of the Ministry of Education & Human Resources Development in Korea
- Oxidative stress;
- Protein tyrosine phosphatase;
- Vascular apoptosis
We used 2-DE and MALDI-TOF/TOF to identify proteins of vascular smooth muscle cells whose expression was or was not altered by exposure to 500 μM H2O2 for 30 min. We detected more than 800 proteins on silver-stained gels of whole protein extracts from rat aortic smooth muscle strips. Of these proteins, 135 clearly unaffected and 19 having levels altered by exposure to H2O2 were identified. Protein characterization revealed that the most prominent vascular smooth muscle proteins were those with antioxidant, cytoskeletal structure, or muscle contraction. In addition, cofilin, an isoform of the actin depolymerizing factor family, shifted to its basic site on the 2-DE gel as a result of H2O2 treatment. In Western blot analysis of proteins from A7r5 aortic smooth muscle cells, the phosphorylation, but not the expression, of cofilin was decreased by H2O2 in a dose-dependent manner. The H2O2-induced dephosphorylation of cofilin and apoptosis was inhibited by Na3VO4, an inhibitor of protein tyrosine phosphatase (PTP). These results suggest that cofilin is one of the proteins regulated by H2O2 treatment in vascular smooth muscle, and has an important role in the induction of vascular apoptosis through PTP-dependent mechanisms.