| First Author | Raman KG | Year | 2006 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 291 |
| Issue | 4 | Pages | G556-65 |
| PubMed ID | 16751175 | Mgi Jnum | J:116894 |
| Mgi Id | MGI:3695195 | Doi | 10.1152/ajpgi.00055.2006 |
| Citation | Raman KG, et al. (2006) The role of RAGE in the pathogenesis of intestinal barrier dysfunction after hemorrhagic shock. Am J Physiol Gastrointest Liver Physiol 291(4):G556-65 |
| abstractText | The receptor for advanced glycation end products (RAGE) has been implicated in the pathogenesis of numerous conditions associated with excessive inflammation. To determine whether RAGE-dependent signaling is important in the development of intestinal barrier dysfunction after hemorrhagic shock and resuscitation (HS/R), C57Bl/6, rage(-/-), or congenic rage(+/+) mice were subjected to HS/R (mean arterial pressure of 25 mmHg for 3 h) or a sham procedure. Twenty-four hours later, bacterial translocation to mesenteric lymph nodes and ileal mucosal permeability to FITC-labeled dextran were assessed. Additionally, samples of ileum were obtained for immunofluorescence microscopy, and plasma was collected for measuring IL-6 and IL-10 levels. HS/R in C57Bl/6 mice was associated with increased bacterial translocation, ileal mucosal hyperpermeability, and high circulating levels of IL-6. All of these effects were prevented when C57Bl/6 mice were treated with recombinant human soluble RAGE (sRAGE; the extracellular ligand-binding domain of RAGE). HS/R induced bacterial translocation, ileal mucosal hyperpermeability, and high plasma IL-6 levels in rage(+/+) but not rage(-/-) mice. Circulating IL-10 levels were higher in rage(-/-) compared with rage(+/+) mice. These results suggest that activation of RAGE-dependent signaling is a key factor leading to gut mucosal barrier dysfunction after HS/R. |
