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. Author manuscript; available in PMC: 2016 Feb 5.
Published in final edited form as: Brain Res. 2015 Mar 3;1623:81–96. doi: 10.1016/j.brainres.2015.02.045

Table 1.

Articles studying circulating cells response in diabetic stroke models

Author Animal model Stroke model Circulating cells response Stroke outcome Follow up time
(Ritter et al., 2011) Zucker Diabetic Fatty (ZDF) rats – type 2 diabetic Intraluminal filament model - 2 h MCAO Increased neutrophil activation, adhesion and decreased shear rate. Increased expression of CD11b and sICAM Worse infarct size and neurologic function. 4 h after reperfusion
(Chen et al., 2011a) Type 2 diabetic db/db mice Intraluminal filament model - Permanent MCAO In diabetic animals, BM-derived EPCs were reduced and dysfunctional as measured by reduced tube formation ability in vitro. The levels of circulating EPC-MPs and EMPs were increased in db/db mice. Larger infarct volume 48 h after MCAO
(Kim et al., 2014) Diet induced type 2 diabetes in mice Intraluminal filament model - 30 min MCAO Increased MCP-1 expression in peritoneal immune cells. Blunted inflammatory response in diabetic brain manifested by decreased MCP-1 RNA. Attenuated LPS-stimulated inflammatory response in macrophages. Exacerbate d ischemic brain injury and infarct. 3 days post ischemia

MCAO: middle cerebral artery occlusion; CD11b: cluster of differentiation molecule b; sICAM; soluble intercellular adhesion molecule; BM: bone marrow; EPCs: endothelial progenitor cells; EPC-MPs; endothelial progenitor cell-derived microparticles; MCP-1: monocyte chemoattractant protein 1; LPS: lipopolysaccharide.

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