Microparticles mediate hepatic ischemia-reperfusion injury and are the targets of Diannexin (ASP8597).

ABSTRACT:

Background & aims

Ischemia-reperfusion injury (IRI) can cause hepatic failure after liver surgery or transplantation. IRI causes oxidative stress, which injures sinusoidal endothelial cells (SECs), leading to recruitment and activation of Kupffer cells, platelets and microcirculatory impairment. We investigated whether injured SECs and other cell types release microparticles during post-ischemic reperfusion, and whether such microparticles have pro-inflammatory, platelet-activating and pro-injurious effects that could contribute to IRI pathogenesis.

Methods

C57BL6 mice underwent 60 min of partial hepatic ischemia followed by 15 min-24 hrs of reperfusion. We collected blood and liver samples, isolated circulating microparticles, and determined protein and lipid content. To es

SUBMITTER: Teoh NC 

PROVIDER: S-EPMC4164362 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature