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1 Cell Biology, Institute of Molecular Biology, Austrian Academy of Sciences, Salzburg, Austria
2 Cell Biology, Institute of Molecular Biology, Austrian Academy of Sciences, Salzburg, Austria; Cell Biology and Oncology, Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy
* To whom correspondence should be addressed. E-mail: gimona{at}dcbo.negrisud.it.
The migration of vascular smooth muscle cells (VSMCs) is a principal factor for the development and progression of vascular diseases. In addition, phenotypic alteration from the contractile (differentiated) to the synthetic (dedifferentiated) state, and a proteolytic process in the form of extra cellular matrix degradation are necessary for SMC invasion. The actual mechanism leading to SMC migration within the tissue itself is, however, unclear. In response to phorbol ester (PDBu) VSMCs in culture form podosomes dynamic organelles critical for cell adhesion and substrate degradation and which are typically found in invasive cells and cells that cross tissue boundaries. Here we show that PDBu-stimulated VSMCs resorb extracellular matrix at the sites of podosomes. Podosome formation correlates with an increased polarization of VSMCs on fibronectin or collagen-coated flexible substrates, in addition to a concomitant induction of cell motility. VSMCs embedded in reconstituted basement membrane support adopt the typical spindle shaped morphology of differentiated smooth muscle cells in vivo and, following PDBu treatment, form peripheral lamellipodia, and podosomes around their matrix-contacting surface. Our findings demonstrate that podosome formation is the potential mechanism underlying the ability of VSMCs to traverse the surrounding basement membrane and escape the barrier of the tunica media in vascular diseases.
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