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Cardiovascular Research 2006 69(3):755-763; doi:10.1016/j.cardiores.2005.12.001
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Copyright © 2005, European Society of Cardiology

Fibulin-2 is present in murine vascular lesions and is important for smooth muscle cell migration

Åsa Ströma,*, Anders I. Olinb, Anders Aspbergc and Anna Hultgärdh-Nilssona

aDepartment of Experimental Medical Science, Division of Vascular and Airway Research, Lund University, BMC, C12, S-221 84 Lund, Sweden
bDepartment of Clinical Sciences, Division of Clinical and Experimental Infectious Medicine, Lund University, Sweden
cDepartment of Experimental Medical Science, Division of Cell and Matrix Biology, Lund University, Sweden

* Corresponding author. Tel.: +46 2229672; fax: +46 2113417. Email address: asa.strom{at}med.lu.se

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.

KEYWORDS Fibulin-2; Versican; Extracellular matrix; Atherosclerosis; Smooth muscle cells

Time for primary review 24 days


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