Dual ablation of integrin α11 and syndecan-4 attenuates cardiac hypertrophy in response to increased left ventricular afterload and reduces cell attachment to extracellular matrix components.
Integrin α1 and syndecan-4 are critical, interdependent mediators of the hypertrophic response to increased left ventricular afterload.
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.
Romaine et al. (Fri,) conducted a other in Cardiac hypertrophy. Integrin α11β1 and syndecan-4 dual receptor ablation was evaluated on Cardiac hypertrophy and cell attachment to extracellular matrix components. Dual ablation of integrin α11 and syndecan-4 attenuates cardiac hypertrophy in response to increased left ventricular afterload and reduces cell attachment to extracellular matrix components.