Vascular Injury Induces Expression of Periostin

Abstract

T issue remodeling after injury involves the coordinate regulation of numerous genes, including those involved with extracellular matrix (ECM) synthesis and turnover, cell adhesion, and cell migration. Major components of the ECM include structural proteins and a number of soluble ECMassociated proteins. The soluble ECM-associated proteins include SPARC, lumican, and the fasciclin domain-containing proteins ig-H3 and periostin. Periostin, originally named osteoblast-specific factor-2 (Genbank D13664) was identified as a soluble ECM protein that was expressed in bone and, to a lesser extent, lung.1 The periostin mRNA is alternatively spliced, resulting in polypeptides that differ in the length of their C-terminal domains and in their tissue-specific patterns of expression. 2Periostin is a 90-kDa heparin-binding N-glycosylated protein that was proposed to associate with bone ECM, and it is highly homologous to ig-h3, previously known as the 68-kDa transforming growth factor (TGF)-1-inducible protein. Both periostin and ig-h3 contain 4 tandem fasciclin (Fas1) domains homologous to the insect protein fasciclin. 3 In the case of ig-h3, the second and fourth fasciclin domains interact with the 31 integrin, and all 4 fasciclin domains can interact with the v5 integrin, thus mediating adhesion.4 Periostin also mediates cell adhesion by binding to v3 and v5, and increases cell motility. 5 The localization of recombinant periostin with v5 integrin at sites of focal adhesion 5 suggests the contribution of periostin to cell adhesion and motility. Despite these recent observations of periostin interacting with cell surface receptors, its functional roles are not clear. More recently, periostin expression was found in embryonic hearts by embryonic day E10.5, and increased to a plateau by E14. Periostin mRNA expression was localized to the endocardial cushions that ultimately divide the primitive heart into the mature 4-chambered heart. 6 In addition, periostin expression is increased in pulmonary aortic smooth muscle cells (SMCs)in response to hypoxia. 7The goal of the present study was to examine the role of periostin in SMCs. Our data indicate that periostin is associated with SMC differentiation and functions as a migratory stimulus in vitro. After balloon catheter injury, periostin expression coincides with the proliferative phase of SMCs in the neointima. Methods AnimalsSprague-Dawley rats were used and the left carotid artery and the aorta were denuded with a 2-French balloon catheter as described. Vascular Injury Induces Expression of Periostin Implications for Vascular Cell Differentiation and MigrationVolkhard Lindner, Qiaozeng Wang, Barbara A. Conley, Robert E. Friesel, Calvin P.H. VaryObjective-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 ...

Immunolocalization of chick periostin protein in the developing heart

“…This hypothesis is consistent with the cells of the tooth mesenchyme that also highly express periostin and undergo an EMT (Kruzynska-Frejtag et al, 2004). During cardiovascular development initially, periostin is expressed in response to signaling from the BMP and TGF-␤ family of growth factors (Horiuchi et al, 1999;Ji et al, 2000;Hall et al, 2001;Kruzynska-Frejtag et al, 2001Lindner et al, 2004). However, as development progresses, the heart must withstand the increasing influence of hemodynamic sheer stress (Stekelenburg et al, 2004).…”

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the β4 integrin and the PI3k pathway

“…It is now generally accepted that tumour cells modify the composition of the adjacent stroma by secreting their own extracellular matrix proteins to create a permissive and supportive environment for their growth (Bissell and Radisky, 2001;Koninger et al, 2004). This hypothesis is supported by the observation that periostin transcription is upregulated in pulmonary smooth muscle cells exposed to hypoxic conditions (Li et al, 2004), in damaged myocardial tissues where migration and resistance of cells to apoptosis is essential (Lindner et al, 2005;Litvin et al, 2005) and in the area around developing teeth where intense cell traction and cell stress occur (Rios et al, 2005). Altogether, these data demonstrate that gain of adhesive interaction induced by overexpression of periostin through the desmoplastic stroma should confer to the cancer cells a selective advantage during the metastatic process and suggest that periostin could be considered as a new member of the matricellular family.…”

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

“…In the same context, we recently found that the expression of βig-h3 in cultured human monocyte-derived macrophages can be induced by tumor necrosis factor-α or IL-1β, inflammatory cytokines frequently increased in atherosclerotic microenvironment (data not published). Periostin, a matrix protein that is highly homologous to βig-h3, is also elevated in rat arteries after vascular injury and localized to smooth muscle cells of the neointima and adventitia and promotes migration of VSMCs (Lindner et al, 2005). Fas-1 domains of βig-h3 and related proteins such as periostin, stabilin-1, and stabilin-2 have been shown to interact with integrins and modulate cell adhesion and migration (Gillan et al, 2002;Kim et al, 2002;Politz et al, 2002).…”