Hyaluronan Fragments Promote Inflammation by Down-Regulating the Anti-inflammatory A2a Receptor

• DOI: 10.1165/rcmb.2010-0387oc
• Publication Date: 2011-01-22T04:04:48Z
• Authors: Samuel L. Collins; Katharine E. Black; Yee Chan-Li; Young-Hoon Ahn; Philip A. Cole; Jonathan D. Powell; Maureen R. Horton
• Keywords: Adenosine A2A receptor

The tissue microenvironment plays a critical role in regulating inflammation. Chronic inflammation leads to an influx of inflammatory cells and mediators, extracellular matrix turnover, increased adenosine. Low molecular weight (LMW) fragments hyaluronan (HA), component, play lung fibrosis by inducing gene expression at the injury site. Adenosine, crucial negative regulator inflammation, protects tissues from immune destruction via adenosine A2a receptor (A2aR). Therefore, these two products opposing roles responses. As such, we wanted determine effect LMW HA on A2aR function. In this article, demonstrate that causes rapid, significant, sustained down-regulation A2aR. CD44 was found be necessary for down-modulate as protein kinase C signaling. We also induces during vivo, can blocked treatment with HA-blocking peptide. Because limiting our data provide novel mechanism whereby itself may further augment By defining pro- anti-inflammatory properties components, will better able identify specific pharmacologic targets potential therapies.