Integrin α11β1 and syndecan-4 dual receptor ablation attenuate cardiac hypertrophy in the pressure overloaded heart
Andreas Romaine, Arne Olav Melleby, Jahedul Alam, Viola Hélène Lobert, Ning Lü, Francesca Lockwood, Almira Hasic, Ida G. Lunde, Ivar Sjaastad, Harald Stenmark, Kate M. Herum, Donald Gullberg, Geir Christensen
Abstract
Despite their putative importance in stress sensing, the specific integrin α-subunit(s) involved in cardiac hypertrophy has not been identified. Here, we show that α11 and syndecan-4 are critical and interdependent mediators of the hypertrophic response to increased LV afterload. We demonstrate in cells lacking both receptors an interdependent reduction in cell attachment to the major cardiac extracellular matrix components, suggesting that their interplay represents an important mechanism for stress sensing in cardiac cells.
Topics & Concepts
CardiologyInternal medicineCardiac hypertrophySyndecan 1MedicineAblationMuscle hypertrophyIntegrinReceptorChemistryCellBiochemistryCardiac Fibrosis and RemodelingTissue Engineering and Regenerative MedicineCardiovascular Function and Risk Factors