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SARM1mediates TLR9-induced vascular hyperpermeability following hemorrhagic shock

 
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Research Article  
dx.doi.org/10.18081/2333-5106/015-10/644-657
American Journal of BioMedicine Volume 3, Issue 10, pages 644-657
Published: October 25, 2015


Morrison R. Doellea, Benjamin M. Predmore, Adrienne A. Kiss, Henri A. Leuvenink, Robert Clements mail of corresponding author

Abstract

Hemorrhagic shock (HS) result in multiple organ dysfunction syndrome (MODS) and inflammatory response. It is one of the world's leading causes of death within the first 40 years of life and thus a significant health problem. The exact mechanism is not clear. TLRs are stimulated both by pathogen-associated molecular patterns as well as by damage-associated molecular patterns, including trauma and hemorrhagic shock. In the present study, we investigated whether the SARM1 responsible for mediats-TLR9-induces inflammatory process and vascular hyperpermeability following hemorrhagic shock. Here we produced an in vivo model of severe hemorrhagic shock in adult wild type mice (40 ± 2 mmHg for 90 min, fluid resuscitation for 30 min) was employed. Mesenteric postcapillary venules were examined for changes in hyperpermeability by intravital microscopy. Blood samples were collected for measurement of tumor necrosis factor (TNF) using ELISA. Biopsies were obtained from organs for light microscopic examination. Our data suggest that SARM1 promising a new mechanisim of TLR9 involved in regulation of hemorrhagic shock and therapeutic target for the treatment of hemorrhagic shock.

Keywords: Hemorrhagic shock; Inflammatory response; SARM1; TLR9

Copyright © 2015 by The American Society for BioMedicine and BM-Publisher, Inc.

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