The Latest RAGE in Restinosis
Expansion of the neointima is a problem in chronic atherosclerosis as well as in response to acute arterial injury. Smooth muscle cells (SMCs) play a key role in the pathologic extension of the neointima that ultimately impinges on the vascular lumen. RAGE, the receptor for advanced glycation end products, is upregulated at sites of vascular pathology, and its blockage is beneficial in mouse atherosclerosis models. Yoshifumi Naka and colleagues have examined RAGE's role in acute arterial injury. As they report (pages 959972), inhibition of RAGE suppressed neointimal formation in mice upon arterial injury and decreased SMC proliferation, migration, and expression of ECM proteins. Inhibition of RAGE specifically in SMCs yielded similar results. The data point to a key role for RAGE in regulating SMCs after arterial injury and suggest the receptor as a target for therapeutic intervention in heart disease.
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Spreading Mucosal Immunity
Local mucosal immunization leads to antigen-specific IgA production at distant mucosal sites, presumably through the migration of activated B cells. Because of the important implications for vaccine development, Eric Kunkel and colleagues are working to understand the mechanisms of IgA-secreting B cell trafficking between distant mucosal sites. Having previously identified a chemokine called MEC, which is expressed by epithelial cells in a variety of mucosal tissues, they report now (pages 10011010) that the MEC-binding chemokine receptor CCR10 is expressed on IgA-secr
Contact: Brooke Grindlinger
Journal of Clinical Investigation