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1 Anatomy and Cell Biology, Temple Medical School, Philadelphia, Pennsylvania, United States
2 Physiology, Temple Medical School, Philadelphia, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: judith.litvin{at}temple.edu.
In injured blood vessels activated VSMCs migrate from the media to the intima, proliferate and synthesize matrix proteins. This results in occlusion of the lumen and detrimental clinical manifestations. We have identified a novel isoform of the periostin family of proteins referred to as Periostin-Like-Factor (PLF). PLF expression in vascular smooth muscle cells (VSMC) was increased following treatment with mitogenic compounds, suggesting that PLF plays a role in VSMC activation. Correspondingly, proliferation of the cells was significantly reduced with anti-PLF antibody treatment. PLF expression increased VSMC migration, an essential cellular process leading to vascular restenosis after injury. PLF protein was localized to neointimal VSMC of rat and swine balloon angioplasty injured arteries, as well as in human arteries with transplant restenosis, supporting the hypothesis that PLF is involved in VSMC activation and vascular proliferative diseases. Taken together, these data suggest a role for PLF in the regulation of vascular proliferative disease.
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