| First Author | Friedrich EB | Year | 2006 |
| Journal | Biochem Biophys Res Commun | Volume | 349 |
| Issue | 3 | Pages | 883-9 |
| PubMed ID | 16962068 | Mgi Jnum | J:113091 |
| Mgi Id | MGI:3664492 | Doi | 10.1016/j.bbrc.2006.07.217 |
| Citation | Friedrich EB, et al. (2006) Role of integrin-linked kinase in vascular smooth muscle cells: regulation by statins and angiotensin II. Biochem Biophys Res Commun 349(3):883-9 |
| abstractText | Our goal was to characterize the role of integrin-linked kinase (ILK) in vascular smooth muscle cells (VSMC), which play a crucial role in atherogenesis. Transfection of VSMC with wild-type and dominant-negative ILK cDNA constructs revealed that ILK mediates migration and proliferation of VSMC but has no effect on VSMC survival. The pro-atherogenic mediator angiotensin II increases ILK protein expression and kinase activity while statin treatment down-regulates ILK in VSMC. Functionally, ILK is necessary for angiotensin II-mediated VSMC migration and proliferation. In VSMC transduced with dominant-negative ILK, statins mediate an additive inhibition of VSMC migration and proliferation, while transfection with wild-type ILK is sufficient to overcome the inhibitory effects of statin treatment on VSMC migration and proliferation. In vivo, ILK is expressed in VSMC of aortic sections from wild-type mice where it is down-regulated following statin treatment and up-regulated following induction of atherosclerosis in apoE-/- mice. These data identify ILK as a novel target in VSMC for anti-atherosclerotic therapy. |
