Expression of vascular endothelial growth factor and its receptors in rat neural stem cells

Maurer, Martin H.; Tripps, Wolf K.C.; Feldmann, Robert; Kuschinsky, Wolfgang

doi:10.1016/s0304-3940(03)00407-5

Cited by 131 publications

(111 citation statements)

References 21 publications

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“…A precedent for an indirect effect vis-à-vis VEGFinduced neurogenesis is the seasonal addition of new neurons to the high vocal center (HVC) of male songbirds, in which testosterone-induced VEGF was found to stimulate nearby endothelial cells to secrete BDNF that, in turn, promotes recruitment of neurons from the HVC ventricular zone (24). The notion of a direct response of neurons to VEGF is supported by reports on expression of the high-affinity VEGF receptors FLK1 and FLT1 and of the auxiliary nonsignaling receptor neuropilin on neuronal cells (6,(25)(26)(27). Also consistent with a direct mechanism are findings showing that VEGF can induce neurite growth in cultured cortical neurons (28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Reversible modulations of neuronal plasticity by VEGF

Licht

Goshen

Avital

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

217

191

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Neurons, astrocytes, and blood vessels are organized in functional “neurovascular units” in which the vasculature can impact neuronal activity and, in turn, dynamically adjust to its change. Here we explored different mechanisms by which VEGF, a pleiotropic factor known to possess multiple activities vis-à-vis blood vessels and neurons, may affect adult neurogenesis and cognition. Conditional transgenic systems were used to reversibly overexpress VEGF or block endogenous VEGF in the hippocampus of adult mice. Importantly, this was done in settings that allowed the uncoupling of VEGF-promoted angiogenesis, neurogenesis, and memory. VEGF overexpression was found to augment all three processes, whereas VEGF blockade impaired memory without reducing hippocampal perfusion or neurogenesis. Pertinent to the general debate regarding the relative contribution of adult neurogenesis to memory, we found that memory gain by VEGF overexpression and memory impairment by VEGF blockade were already evident at early time points at which newly added neurons could not yet have become functional. Surprisingly, VEGF induction markedly increased in vivo long-term potentiation (LTP) responses in the dentate gyrus, and VEGF blockade completely abrogated LTP. Switching off ectopic VEGF production resulted in a return to a normal memory and LTP, indicating that ongoing VEGF is required to maintain increased plasticity. In summary, the study not only uncovered a surprising role for VEGF in neuronal plasticity, but also suggests that improved memory by VEGF is primarily a result of increasing plasticity of mature neurons rather than the contribution of newly added hippocampal neurons.

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Section: Discussionmentioning

confidence: 99%

Reversible modulations of neuronal plasticity by VEGF

Licht

Goshen

Avital

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

217

191

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“…During brain development, the ventricular neuroectoderm produces VEGF, which promotes vessel growth (Breier et al, 1992;Raab et al, 2004). Adult SVZ neural progenitor cells express many angiogenic factors, including VEGF and its receptors (Liu et al, 2007;Maurer et al, 2003;Rafuse et al, 2005;Tonchev et al, 2007). Stroke upregulates angiogenic genes in SVZ cells (Liu et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Coupling of Angiogenesis and Neurogenesis in Cultured Endothelial Cells and Neural Progenitor Cells after Stroke

Hua

Zhang

Wang

et al. 2007

J Cereb Blood Flow Metab

226

176

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Angiogenesis and neurogenesis are coupled processes. Using a coculture system, we tested the hypothesis that cerebral endothelial cells activated by ischemia enhance neural progenitor cell proliferation and differentiation, while neural progenitor cells isolated from the ischemic subventricular zone promote angiogenesis. Coculture of neural progenitor cells isolated from the subventricular zone of the adult normal rat with cerebral endothelial cells isolated from the stroke boundary substantially increased neural progenitor cell proliferation and neuronal differentiation and reduced astrocytic differentiation. Conditioned medium harvested from the stroke neural progenitor cells promoted capillary tube formation of normal cerebral endothelial cells. Blockage of vascular endothelial growth factor receptor 2 suppressed the effect of the endothelial cells activated by stroke on neurogenesis as well as the effect of the supernatant obtained from stroke neural progenitor cells on angiogenesis. These data suggest that angiogenesis couples to neurogenesis after stroke and vascular endothelial growth factor likely mediates this coupling.

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“…Purity was checked by the ratio of 260-to 280-nm absorptions. For VEGFR-2 mRNA detection, reverse transcription was performed on 2 g of RNA extracts with AMV Reverse Transcriptase (Promega) for first-strand cDNA synthesis, and PCR amplification was obtained in the presence of specific primer pairs [forward primer: 5Ј-CGATGTCTCCTCCATCGTTT-3Ј; reverse primer: 5Ј-TTCCATCCGGAACAAATCTC-3Ј, as described previously by Maurer et al (24)] and Tfl polymerase (Promega) in a protocol of initial denaturation at 94°C for 2 min, 35 cycles of amplification with denaturation at 94°C for 30 s, annealing at 60°C for 1 min, 2 min at 68°C, and final extension for 7 min. Amplification products were visualized by 1% agarose gel electrophoresis.…”

Section: H]thymidine Incorporation and 5-bromo-2ј-deoxyuridine Labelingmentioning

confidence: 99%

Effects of vascular endothelial growth factor on isolated fetal alveolar type II cells

Raoul¹,

Chailley‐Heu²,

Barlier-Mur³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Previous investigations gained from in vivo or lung explant studies suggested that VEGF is an autocrine proliferation and maturation factor for developing alveolar type II cells. The objective of this work was to determine whether VEGF exerted its growth and maturation effects directly on isolated type II cells. These were isolated from 19-day fetal rat lung and cultured in defined medium. The presence of VEGF receptor-2 was assessed in cultured cells at the pre- and posttranslational levels. Recombinant VEGF165, formerly found to be active on lung explants, failed to enhance type II cell proliferation estimated by thymidine and 5-bromo-2′-deoxy-uridine incorporation. It increased choline incorporation in saturated phosphatidylcholine by 27% but did not increase phospholipid surfactant pool size. VEGF (100 ng/ml) left unchanged the transcript level of surfactant proteins (SP)-A, SP-C, and SP-D but increased SP-B transcripts to four times the control steady-state level. VEGF slightly retarded, but did not prevent, the in vitro transdifferentiation of type II into type I cells, as assessed by immunolabeling of the type I cell marker T1α. We conclude that, with the exception of SP-B expression, which appears to be controlled directly, the previously observed effects of this VEGF isoform on type II cells are likely to be exerted indirectly through reciprocal paracrine interactions involving other lung cell types.

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Expression of vascular endothelial growth factor and its receptors in rat neural stem cells

Cited by 131 publications

References 21 publications

Reversible modulations of neuronal plasticity by VEGF

Reversible modulations of neuronal plasticity by VEGF

Coupling of Angiogenesis and Neurogenesis in Cultured Endothelial Cells and Neural Progenitor Cells after Stroke

Effects of vascular endothelial growth factor on isolated fetal alveolar type II cells

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