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| Content Provider | Journal of Biological Chemistry (JBC) |
|---|---|
| Author | Murdoch, Colin E. Shuler, Michaela Haeussler, Dagmar J. F. Kikuchi, Ryosuke Bearelly, Priyanka Han, Jingyan Watanabe, Yosuke Fuster, José J. Walsh, Kenneth Ho, Ye-Shih Bachschmid, Markus M. Cohen, Richard A. Matsui, Reiko |
| Abstract | Glutaredoxin-1 (Glrx) is a cytosolic enzyme that regulates diverse cellular function by removal of GSH adducts from S-glutathionylated proteins including signaling molecules and transcription factors. Glrx is up-regulated during inflammation and diabetes, and Glrx overexpression inhibits VEGF-induced EC migration. The aim was to investigate the role of up-regulated Glrx in EC angiogenic capacities and in vivo revascularization in the setting of hind limb ischemia. Glrx-overexpressing EC from Glrx transgenic (TG) mice showed impaired migration and network formation and secreted higher levels of soluble VEGF receptor 1 (sFlt), an antagonizing factor to VEGF. After hind limb ischemia surgery Glrx TG mice demonstrated impaired blood flow recovery, associated with lower capillary density and poorer limb motor function compared with wild type littermates. There were also higher levels of anti-angiogenic sFlt expression in the muscle and plasma of Glrx TG mice after surgery. Noncanonical Wnt5a is known to induce sFlt. Wnt5a was highly expressed in ischemic muscles and EC from Glrx TG mice, and exogenous Wnt5a induced sFlt expression and inhibited network formation in human microvascular EC. Adenoviral Glrx-induced sFlt in EC was inhibited by a competitive Wnt5a inhibitor. Furthermore, Glrx overexpression removed GSH adducts on p65 in ischemic muscle and EC and enhanced NF-κB activity, which was responsible for Wnt5a-sFlt induction. Taken together, up-regulated Glrx induces sFlt in EC via NF-κB-dependent Wnt5a, resulting in attenuated revascularization in hind limb ischemia. The Glrx-induced sFlt explains part of the mechanism of redox-regulated VEGF signaling. |
| Related Links | http://www.jbc.org/content/289/12/8633.abstract |
| Ending Page | 8644 |
| Starting Page | 8633 |
| Page Count | 12 |
| File Format | HTM / HTML PDF |
| ISSN | 00219258 |
| Journal | Journal of Biological Chemistry (JBC) |
| Issue Number | 12 |
| Volume Number | 289 |
| DOI | 10.1074/jbc.M113.517219 |
| e-ISSN | 1083351X |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology |
| Publisher Date | 2014-03-21 |
| Access Restriction | Open |
| Subject Keyword | Angiogenesis Animal Models Glutathionylation Ischemia NF-kappa B (NF-κB) Redox Regulation Vascular Endothelial Growth Factor (VEGF) Gene Regulation |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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