Notably, genetic interaction between <i>RhoA</i> and <i>SHP2</i> indicated that RhoA inactivation and <i>SHP2</i> deletion synergistically attenuated the allergen-induced eosinophil infiltration into lungs and airway hyperreactivity, whereas overexpression of active RhoA robustly restored the <i>SHP2</i> deletion-resultant attenuation of allergen-induced eosinophil recruitment into lungs and airway hyperreactivity as well.
These data indicate that Mfge8 binding to integrin receptors on ASM opposes the effect of allergic inflammation on RhoA activity and identify a pathway for specific inhibition of ASM hypercontractility in asthma.