Litvin Judith, Chen Xing, Keleman Sheri, Zhu Shimei, Autieri Michael
Temple University, School of Medicine, Department of Anatomy and Cell Biology, 3420 N. Broad St., MRB 615, Philadelphia, PA 19140, USA.
Am J Physiol Cell Physiol. 2007 May;292(5):C1672-80. doi: 10.1152/ajpcell.00153.2006. Epub 2006 Nov 8.
In injured blood vessels activated vascular smooth muscle cells (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 VSMCs 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.
