High impact information on POSTN

• Periostin promotes atrioventricular mesenchyme matrix invasion and remodeling mediated by integrin signaling through Rho/PI 3-kinase [1].
• Both matrix invasion and compaction were associated with a colocalization of periostin and beta(1) integrin expression to migratory cell phenotype in both surface and deep cells [1].
• At HH25, periostin was detected on the basal surface of the trabecular endothelium and also on the endocardial epithelium of the atrioventricular cushion [2].
• Enhanced secretion of periostin in the region of delamination may directly or indirectly promote change in the myocardium that precedes or mediates delamination of the leaflet [2].
• At later stages of development (HH34-38), periostin was seen predominantly in the fibrous regions of the heart, such as the left atrioventricular valve (LAV), annulus, cardiac skeleton, and adventitia [2].

Biological context of POSTN

• Cardiac expression continues into fetal development where periostin is seen predominantly in the valve leaflets and supporting chordae tendinae [3].
• As these molecules are indispensable for cardiac development, we sought to clone the chicken ortholog of periostin and evaluate its spatiotemporal expression pattern during heart morphogenesis [3].
• Periostin, a member of the fasciclin gene family, acts as a cell adhesion molecule through binding to cell surface integrins [3].

Anatomical context of POSTN

• Periostin overexpression resulted in enhanced mesenchyme invasion through 3D collagen gels and increased matrix compaction [1].
• We show by Northern analysis, whole mount and section in situ hybridization experiments that periostin is predominantly expressed in the developing endothelium of the ventricular trabeculae as well as in the endothelium and mesenchyme of the outflow tract and atrioventricular endocardial cushions [3].

Other interactions of POSTN

• Periostin expression has previously been shown to increase substantially following transforming growth factor beta (TGF-beta) and bone morphogenetic protein stimulation [3].

References