Recently, R. Palanivel et al. investigated the role that RhoA-mediated re-organization of the actin cytoskeleton has in adiponectin-regulated glucose uptake in cardiomyocytes.¬ Adiponectin is a protein secreted by adipose tissue that modulates glucose and fatty acid metabolism.¬† In concert with APPL1, an adiponectin receptor binding partner, adiponectin carries out these functions which are important in obesity and type 2 diabetes, two diseases that reduce cardiac energy metabolism. The authors found that adiponectin (both full-length and globular) elevates RhoA activity which correlates with increased actin polymerization and glucose uptake.¬† Changes in the G-/F-actin ratio likely involve APPL1 as adiponectin increases colocalization of actin and APPL1.¬† Inhibition of actin polymerization or RhoA signaling significantly reduces the adiponectin-mediated increase in glucose uptake.¬† Thus, RhoA-mediated actin cytoskeleton remodeling is required for adiponectin-regulated glucose uptake in cardiomyocytes.¬† Increased glucose uptake is cardioprotective in diabetes. A number of products by¬†Cytoskeleton Inc. (“The Protein Experts”)¬ were essential in this study, providing accurate and sensitive assays for quantifying levels of activated RhoA and changes in G- and F-actin levels or binding partners in cardiomyocytes under conditions of RhoA inhibition.
- RhoA G-LISA activation assay¬
- G-/F-actin In Vivo Assay Kit
- Anti-actin antibody
- Cell-permeable Rho inhibitor
These reagents¬†are available in Europe through tebu-bio, who have also compiled¬†useful selection tools:
Reference: Palanivel et al. 2014. Adiponectin stimulates Rho-mediated actin cytoskeleton remodeling and glucose uptake via APPL1 in primary cardiomyocytes. Metabolism. 63, 1363-1373.