The expressions of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 9 (MMP-9) were supposed to show the changing circumstances for neural generation under cerebral ischemia.
While Sesn2, Nrf2, HO-1, and VEGF were significantly increased following cerebral ischemia, overexpression of Sesn2 further increased their expression.
EPO promotes VEGE and its receptor (KDR) expression and participates in the regulation of HIF-1α and eNOS protein expression through the activation of AMPK-KLF2 signaling pathways to promote new vascular development after cerebral ischemia.
Here, OGD-PBMCs were identified to secrete remodelling factors, including the vascular endothelial growth factor and transforming growth factor-β in vitro, while intra-arterial administration of OGD-PBMCs at 7 days after focal cerebral ischemia prompted expression of such factors in the brain parenchyma at 28 days following focal cerebral ischemia in vivo.
Enzyme-linked immunosorbent assay (ELISA) was performed to determine the level of vascular endothelial growth factor (VEGF) in the serum of CI patients.
The aim of this study was to investigate whether miR-490 was involved in the regulation of angiogenesis after cerebral infarction by regulating vascular endothelial growth factor (VEGF) expression.
A previous in vivo study demonstrated that intracerebroventricular injection of basic fibroblast growth factor (bFGF) in middle cerebral artery occlusion rats increased the expression of caveolin-1 (cav-1) and vascular endothelial growth factor (VEGF) in cerebral ischemia penumbra.
These results demonstrated that liraglutide promoted angiogenesis and long-term recovery of cerebral ischemia through increasing the expression of VEGF.
Our data demonstrated that hypoxic preconditioning increased BBB disruption through a VEGF related pathway and suggest the possibility of aggravation of brain edema by hypoxic preconditioning in the early stages of cerebral ischemia.
Taken together, the results indicate that early inhibition of VEGF may have significant potential against cerebral ischemia, partly by regulating the expression of MMPs.
Role of caveolin-1/vascular endothelial growth factor pathway in basic fibroblast growth factor-induced angiogenesis and neurogenesis after treadmill training following focal cerebral ischemia in rats.
Transplantation of BMSCs stably expressing mutant HIF1α significantly improved motor function, reduced cerebral infarction and increased VEGF protein expression revascularization at days 7, 14 and 28 (p<0.05).
This study tested the hypothesis that neuropilin-1 (NP-1), an alternative VEGF receptor, regulates the response to cerebral ischemia by modulating PARP expression and, in turn, apoptosis inhibition by VEGF.
These data suggested that the -1154/, 936/ and -2578/ ACC haplotype was associated with the risk of acute cerebral infarction with an OR of 0.361, and it may reduce the risk of acute cerebral infarction through the regulation of VEGF expression.
Intraventricular pre-treatment with rAAV-VEGF induces intracranial hypertension and aggravates ischemic injury at the early stage of transient focal cerebral ischemia in rats.
In vivo, VEGF controls the correct migration of facial branchiomotor neurons in the developing hindbrain and stimulates the proliferation of neural stem cells in enriched environments and after cerebral ischemia.
Several reports recently suggested that vascular endothelial growth factor (VEGF) may have a therapeutic benefit against experimental cerebral infarction animal models.