Hypoxia-induced vascular endothelial growth factor expression precedes neovascularization after cerebral ischemia
Open accessAbstract
We investigated the hypothesis that hypoxia induces angiogenesis and thereby may counteract the detrimental neurological effects associated with stroke. Forty-eight to seventy-two hours after permanent middle cerebral artery occlusion we found a strong increase in the number of newly formed vessels at the border of the infarction. Using the hypoxia marker nitroimidazole EF5, we detected hypoxic cells in the ischemic border of the neocortex. Expression of vascular endothelial growth factor (VEGF), which is the main regulator of angiogenesis and is inducible by hypoxia, was strongly up-regulated in the ischemic border, at times between 6 and 24 hours after occlusion. In addition, both VEGF receptors (VEGFRs) were up-regulated at the border after 48 hours and later in the ischemic core. Finally, the two transcription factors, hypoxia-inducible factor-1 (HIF-1) and HIF-2, known to be involved in the regulation of VEGF and VEGFR gene expression, were increased in the ischemic border after 72 hours, suggesting a regulatory function for these factors. These results strongly suggest that the VEGF/VEGFR system, induced by hypoxia, leads to the growth of new vessels after cerebral ischemia. Exogenous support of this natural protective mechanism might lead to enhanced survival after stroke.
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After stroke, angiogenic factors are expressed by neurons and astrocytes, which induce microvascular growth.
“After stroke, angiogenic factors are expressed by neurons and astrocytes, which induce microvascular growth.4,47–50”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [48]
VEGF acting through VEGFR2 induces endothelial proliferation and concurrently upregulates delta-like ligand 4, which signals to microvascular cells in the capillary stalk to downregulate VEGFR2 via Notch 1, preventing uncontrolled capillary sprouting.
“Acting through VEGF receptor 2 (VEGFR2), which is localised at high concentrations at the tip of newly formed capillaries, VEGF induces endothelial proliferation,4,47–49 and concur rently upregulates the transmembrane ligand delta-like ligand 4, which signals to microvascular cells in the capillary stalk, to downregulate VEGFR2 via interaction with its receptor Notch 1, thus pre venting uncontroll”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [48]
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Self-citation
- Authors
- Marti, H. J. H., Bernaudin, M., Bellail, A., Schoch, H., Euler, M., Petit, E., & Risau, W.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2000-03
- Volume
- 156
- Issue
- 3
- Pages
- 965-976
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1876841
- OpenAlex
- W2001500938
- Cited by
- 680
- References
- 71
- Citations by year
- 2026: 14 · 2025: 28 · 2024: 11 · 2023: 13 · 2022: 15 · 2021: 22 · 2020: 21 · 2019: 24 · 2018: 28 · 2017: 24 · 2016: 36 · 2015: 31 · 2014: 31 · 2013: 39 · 2012: 42
- FWCI
- 8.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministerio de Economía y Competitividad
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- hypoxia, vascular endothelial growth factor, angiogenesis, neovascularization, cerebral ischemia, stroke, middle cerebral artery occlusion, VEGF receptors, HIF-1, HIF-2, ischemic border zone, ischemic core, neuroprotection
- MeSH terms
- Animals, Hypoxia, Brain Ischemia, Disease Models, Animal, DNA, DNA-Binding Proteins, Immunohistochemistry, Lymphokines, Neovascularization, Pathologic, Nuclear Proteins, Peptide Initiation Factors, Proto-Oncogene Proteins, RNA, Messenger, Transcription Factors, Up-Regulation, Endothelial Growth Factors, In Situ Hybridization, DNA Primers, Receptors, Growth Factor, Ki-67 Antigen, Platelet Endothelial Cell Adhesion Molecule-1, Reverse Transcriptase Polymerase Chain Reaction, Receptor Protein-Tyrosine Kinases, Receptors, Vascular Endothelial Growth Factor, Vascular Endothelial Growth Factor Receptor-1, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Mice, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit
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