Adenosine metabolized from extracellular ATP ameliorates organ injury by triggering A_2BR signaling.

ABSTRACT:

Background

Trauma and a subsequent hemorrhagic shock (T/HS) result in insufficient oxygen delivery to tissues and multiple organ failure. Extracellular adenosine, which is a product of the extracellular degradation of adenosine 5' triphosphate (ATP) by the membrane-embedded enzymes CD39 and CD73, is organ protective, as it participates in signaling pathways, which promote cell survival and suppress inflammation through adenosine receptors including the A_2BR. The aim of this study was to evaluate the role of CD39 and CD73 delivering adenosine to A_2BRs in regulating the host's response to T/HS.

Methods

T/HS shock was induced by blood withdrawal from the femoral artery in wild-type, global knockout (CD39, CD73, A_2BR) and conditional knockout (in

SUBMITTER: Kelestemur T 

PROVIDER: S-EPMC10339538 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature