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Vascular injury induces expression of periostin: implications for vascular cell differentiation and migration.

Authors: Lindner, V  Wang, Q  Conley, BA  Friesel, RE  Vary, CP 
Citation: Lindner V, etal., Arterioscler Thromb Vasc Biol. 2005 Jan;25(1):77-83. Epub 2004 Oct 28.
Pubmed: (View Article at PubMed) PMID:15514205
DOI: Full-text: DOI:10.1161/01.ATV.0000149141.81230.c6

OBJECTIVE: Periostin mRNA is among the most strongly upregulated transcripts in rat carotid arteries after balloon injury. The goal of the present study was to gain insight into the significance of periostin in the vasculature. METHODS AND RESULTS: Periostin expression after injury was localized to smooth muscle cells of the neointima and the adventitia. The expression of periostin in smooth muscle cells in vitro was not regulated by cytokines such as fibroblast growth factor-2 (FGF-2). In contrast, stimulation of MC3T3-E1 osteoblastic cells, NIH3T3 fibroblasts, or mesenchymal C3H10T1/2 cells with FGF-2 reduced periostin mRNA levels to <5% of controls, whereas conversely bone morphogenetic protein-2 (BMP-2) increased periostin mRNA levels. Periostin expression was induced and maintained during retinoic acid-induced smooth muscle cell differentiation in A404 cells. In addition, overexpression of periostin in C3H10T1/2 cells caused an increase in cell migration that could be blocked with an anti-periostin antibody. CONCLUSIONS: Periostin expression is associated with smooth muscle cell differentiation in vitro and promotes cell migration. Unlike other mesenchymally derived cell lines, periostin expression is not regulated by FGF-2 in smooth muscle cells. This distinction may be useful in discriminating smooth muscle and fibroblast lineages.


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CRRD Object Information
CRRD ID: 10040973
Created: 2015-05-07
Species: All species
Last Modified: 2015-05-07
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.