Repulsive guidance molecule a suppresses angiogenesis after ischemia/reperfusion injury of middle cerebral artery occlusion in rats.

Repulsive guidance molecule a (RGMa) has now emerged as a molecule with pleiotropic roles, including repulsion, adhesion, migration and differentiation in the nervous system. In this study, adult male Sprague-Dawley (SD) rats received 90-min middle cerebral artery occlusion (MCAO) to observe RGMa/neogenin expression sites after ischemia/reperfusion injury and changes in angiogenesis after treatment with RNA interference using RGMa-specific recombinant adenovirus rAd5-shRNA-RGMa (rAd-shRGMa). To clarify how RGMa mediates angiogenesis, the RGMa function-blocking peptide six fibronectin type III (6FNIII) was also administered, and corresponding changes in vascular endothelial growth factor (VEGF), angiopoietin-2 (Ang2), angiopoietin-1 (Ang1), and brain derived neurotrophic factor (BDNF) were determined by western blotting.

Overexpression of Fibulin-5 Attenuates Ischemia/Reperfusion Injury After Middle Cerebral Artery Occlusion in Rats.

Ischemia/reperfusion (I/R) injury after middle cerebral artery occlusion (MCAO) induces detrimental processes such as oxidative stress, inflammation, and apoptosis. All parts of the neurovascular unit are involved in these pathological processes. Fibulin-5 is a 66-kD glycoprotein secreted by various vascular cells, including vascular smooth muscle cells (SMCs), fibroblasts, and endothelial cells.

17-AAG post-treatment ameliorates memory impairment and hippocampal CA1 neuronal autophagic death induced by transient global cerebral ischemia.

Neuro-inflammation plays an important role in global cerebral ischemia (GCI). The 72-kDa heat shock protein (Hsp70) has been reported to be involved in the inflammatory response of many central nervous system diseases. Preclinical findings implicate that 17-allylamino-demethoxygeldanamycin (17-AAG), an anticancer drug in clinical, provide neuroprotection actions in a rat model of traumatic brain injury, and the beneficial effects of 17-AAG were specifically due to up-regulation of Hsp70.