| First Author | Ström A | Year | 2006 |
| Journal | Cardiovasc Res | Volume | 69 |
| Issue | 3 | Pages | 755-63 |
| PubMed ID | 16409997 | Mgi Jnum | J:105710 |
| Mgi Id | MGI:3616366 | Doi | 10.1016/j.cardiores.2005.12.001 |
| Citation | Strom A, et al. (2006) Fibulin-2 is present in murine vascular lesions and is important for smooth muscle cell migration. Cardiovasc Res 69(3):755-63 |
| abstractText | OBJECTIVE: The vascular extracellular matrix (ECM) can affect smooth muscle cell (SMC) adhesion, migration and proliferation-events that are important during the atherosclerotic process. Fibulin-2 is a member of the ECM protein family of fibulins and has been found to cross-link versican/hyaluronan complexes, an ECM network that has been suggested to be important during tissue repair. In this study we have analysed the presence of fibulin-2 in two different models of murine vascular lesions. We have also examined how the fibulin-2/versican network influences SMC migration. METHODS: Presence of fibulin-2 was analysed by immunohistochemistry in atherosclerotic aortas and in mechanically injured carotid arteries from mice. Fibulin-2 protein levels were also studied by Western blotting during rat aortic SMC phenotypic modulation in vitro. The importance of a fibulin-2/versican interaction for SMC migration was studied in the presence of two inhibiting peptides (FN III 3-5 and aggrecan C-type lectin-like domain). RESULTS: Fibulin-2 is expressed in SMC rich regions of atherosclerotic lesions where it colocalises with versican and hyaluronan. It is also present in injury-induced vascular lesions and is upregulated during SMC phenotypic modulation in cell culture. Moreover, treatments with peptides that block the interaction between versican and fibulin-2 inhibit SMC migration in vitro. CONCLUSIONS: Fibulin-2 can be produced by SMC as a response to injury and may participate in the ECM organisation that regulates SMC migration during vessel wall repair. |
