HEM-6: ANALYSIS OF XXXX PLASMA PEPTIDOME IN HEMORRHAGIC SHOCK.

@entity548 @entity63 @entity1457 @entity17937 @entity12186 @entity8683 @entity881 @entity35 @entity204 @entity8682
INTRODUCTION: @entity1457 is a frequent cause of @entity204 and a most important unresolved medical problem. Reduction of blood supply to the intestine during @entity63 disrupts the mucosal epithelial barrier allowing inflammatory materials in the lumen of the intestine, including digestive enzymes, to cross the intestinal wall (Fig. 1). The transport of digestive enzymes leads to uncontrolled digestive enzyme activity in the circulation, which generates cell/tissue damage and a strong inflammatory reaction. Recent studies have demonstrated that the uncontrolled proteolytic activity causes cleavage of important membrane receptors on the endothelial cells (e.g., @entity8683 , @entity12186 and @entity17937 ) and loss of the associated cell functions. So, understanding the contribution of degrading proteases to circulatory shock serves to elucidate the mechanisms leading to @entity881 and to detect potential biomarkers and/or therapeutic targets.(Figure is included in full-text article.) RESULTS: : We performed a label-free quantitative proteomic analysis comparing the peptidome of plasma samples from @entity35 without and with @entity548 to verify the possible role of uncontrolled proteolytic activity (Fig. 2). Peptides were differentially expressed if they were present only in the group without (C) or with @entity548 ( @entity8682 ) or if they had a significant difference in plasma concentration (cut-off values: fold change >1.5 or <0.67). 256 peptides were up-regulated or present only in @entity8682 group, while 60 peptides were down-regulated in the @entity8682 group or were present only in the C group.(Figure is included in full-text article.) CONCLUSION: : Our preliminary results suggest that there is an increase in protease activity into the systemic circulation following @entity548 leading to generation of peptide fragments in plasma.
