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VEGF-induced neuroprotection, neurogenesis, and angiogenesis after focal cerebral ischemia
Yunjuan Sun, … , Anna Logvinova, David A. Greenberg
Yunjuan Sun, … , Anna Logvinova, David A. Greenberg
Published June 15, 2003
Citation Information: J Clin Invest. 2003;111(12):1843-1851. https://doi.org/10.1172/JCI17977.
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Article Neuroscience

VEGF-induced neuroprotection, neurogenesis, and angiogenesis after focal cerebral ischemia

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Abstract

Vascular endothelial growth factor (VEGF) is an angiogenic protein with therapeutic potential in ischemic disorders, including stroke. VEGF confers neuroprotection and promotes neurogenesis and cerebral angiogenesis, but the manner in which these effects may interact in the ischemic brain is poorly understood. We produced focal cerebral ischemia by middle cerebral artery occlusion for 90 minutes in the adult rat brain and measured infarct size, neurological function, BrdU labeling of neuroproliferative zones, and vWF-immunoreactive vascular profiles, without and with intracerebroventricular administration of VEGF on days 1–3 of reperfusion. VEGF reduced infarct size, improved neurological performance, enhanced the delayed survival of newborn neurons in the dentate gyrus and subventricular zone, and stimulated angiogenesis in the striatal ischemic penumbra, but not the dentate gyrus. We conclude that in the ischemic brain VEGF exerts an acute neuroprotective effect, as well as longer latency effects on survival of new neurons and on angiogenesis, and that these effects appear to operate independently. VEGF may, therefore, improve histological and functional outcome from stroke through multiple mechanisms.

Authors

Yunjuan Sun, Kunlin Jin, Lin Xie, Jocelyn Childs, Xiao Ou Mao, Anna Logvinova, David A. Greenberg

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Figure 5

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Effects of intraventricular VEGF on the number of BrdU-labeled neurons i...
Effects of intraventricular VEGF on the number of BrdU-labeled neurons in DG and SVZ, ipsilateral and contralateral to MCAO, at 3 and 28 days after ischemia. For control, aCSF was administered instead of VEGF. Dotted line, basal level of BrdU labeling in normal, nonischemic rats. Two-way ANOVA showed significant effects of location (F = 26.85, P < 0.0001) but not treatment (F = 2.48, P = 0.120) on the number of BrdU-labeled neurons at 3 days after ischemia and of location (F = 22.13, P < 0.0001) and treatment (F = 27.28, P < 0.0001) on the number of BrdU-labeled neurons at 28 days after ischemia, but no interaction between location and treatment at 3 days (F = 1.14, P = 0.340) or 28 days (F = 3.83, P = 0.014). *P < 0.05, **P < 0.01 compared with control on same day at same location (Tukey test; n = 9). DG-I, ipsilateral dentate gyrus; DG-C, contralateral dentate gyrus; SVZ-I, ipsilateral subventricular zone; SVZ-C, contralateral subventricular zone.
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