ArticleGlia2010
In the hypoxic central nervous system, endothelial cell proliferation is followed by astrocyte activation, proliferation, and increased expression of the alpha 6 beta 4 integrin and dystroglycan.
Article in Glia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 75 citations in OpenAlex.
- A central role for fibrinogen in promoting microglial repair of the hypoxia-disrupted blood-brain barrier.Journal of neuroinflammation · 2026Article
- Article
- Endothelial Cell Integrin α6 Regulates Vascular Remodeling Through the PI3K/Akt-eNOS-VEGFA Axis After Stroke.Neuroscience bulletin · 2025Article
- Partial eNOS Deficiency Results in Greater Levels of Vascular Inflammation and BBB Disruption in Response to Chronic Mild Hypoxia.International journal of molecular sciences · 2025Article
- Defining the hypoxic thresholds that trigger blood-brain barrier disruption: the effect of age.Aging · 2025Article
- CX3CR1-Fractalkine Dysregulation Affects Retinal GFAP Expression, Inflammatory Gene Induction, and LPS Response in a Mouse Model of Hypoxic Retinopathy.International journal of molecular sciences · 2025Article
- The importance of laminin at the blood-brain barrier.Neural regeneration research · 2023Review
- Article
- Spinal Cord Blood Vessels in Aged Mice Show Greater Levels of Hypoxia-Induced Vascular Disruption and Microglial Activation.International journal of molecular sciences · 2023Article
- β1 integrin is essential for blood-brain barrier integrity under stable and vascular remodelling conditions; effects differ with age.Fluids and barriers of the CNS · 2023Article
- Hypoxia-induced vascular remodeling responses in the brain are much more robust than other organs.Microvascular research · 2023Article
- The impact of genetic manipulation of laminin and integrins at the blood-brain barrier.Fluids and barriers of the CNS · 2022Review
- Hypoxia increases expression of selected blood-brain barrier transporters GLUT-1, P-gp, SLC7A5 and TFRC, while maintaining barrier integrity, in brain capillary endothelial monolayers.Fluids and barriers of the CNS · 2022Article
- Time Domains of Hypoxia Responses and -Omics Insights.Frontiers in physiology · 2022Review
- Mild hypoxia triggers transient blood-brain barrier disruption: a fundamental protective role for microglia.Acta neuropathologica communications · 2020Article
- Chronic mild hypoxia accelerates recovery from preexisting EAE by enhancing vascular integrity and apoptosis of infiltrated monocytes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Expression of Cellular Receptors in the Ischemic Hemisphere of Mice with Increased Glucose Uptake.Experimental neurobiology · 2020Article
- A critical role for microglia in maintaining vascular integrity in the hypoxic spinal cord.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Chronic Exposure to High Altitude: Synaptic, Astroglial and Memory Changes.Scientific reports · 2019Article
- Angiogenesis in the ischemic core: A potential treatment target?Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Cerebral hypoxia induces a profound angiogenic response in the central nervous system (CNS). Using a mouse model of chronic cerebral hypoxia, we previously demonstrated that angiogenic vessels in the hypoxic CNS show marked upregulation of the extracellular matrix (ECM) protein fibronectin, along with increased expression of its major receptor, alpha 5 beta 1 integrin on brain endothelial cells (BEC). As cerebral hypoxia also leads to glial activation, the aim of the current study was to define the temporal relationship between BEC responses and glial cell activation in this model of cerebral hypoxia. This revealed that BEC fibronectin/alpha 5 beta 1 integrin expression and proliferation both reached maximal level after 4-day hypoxia. Interestingly, up to 4-day hypoxia, all dividing cells were BEC, but at later time-points proliferating astrocytes were also observed. GFAP staining revealed that hypoxia induced marked astrocyte activation that reached maximal level between 7- and 14-day hypoxia. As newly formed cerebral capillaries require ensheathment by astrocyte end-feet to acquire mature brain endothelium characteristics, we next examined how expression of astrocyte end-feet adhesion molecules is regulated by hypoxia. This showed that the astrocyte adhesion receptors alpha 6 beta 4 integrin and dystroglycan were both markedly upregulated, with a time-course that closely resembled astrocyte activation. Taken together, this evidence shows that cerebral hypoxia promotes first an endothelial response, in which fibronectin promotes BEC proliferation. This is then followed by an astrocyte response, involving astrocyte activation, proliferation, and reorganization of astrocyte end-feet, which correlates with increased expression of astrocyte end-feet adhesion molecules.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.