VEGF-mediated disruption of endothelial CLN-5 promotes blood-brain barrier breakdown

By A. Argaw, B. Gurfein, Yueting Zhang, A. Zameer, G. John. Proceedings of the National Academy of Sciences of the United States of America, 2009

659 citations recorded by the source corpus.

Subfields: Cancer Research, Neurology

View Paper: https://www.semanticscholar.org/paper/c2263a385849d8c49c397c462f3e147f39c987d1

How researchers see this paper

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In Cancer Research

1. M. Sofroniew
2. H. Vinters
3. A. Prat
4. N. Ferrara
5. J. Burda
6. R. Daneman
7. Rakesh K. Jain
8. A. Adamis

In Neurology

1. M. Sofroniew
2. M. Pekny
3. J. Burda
4. M. Pekna
5. H. Vinters
6. Alexander M. Bernstein
7. A. Prat
8. Robert S. Pulido

Citations in the corpus

• Tight junctions at the blood brain barrier: physiological architecture and disease-associated dysregulation (2012, positive): “VEGF-mediated Tyr-phosphorylation of TJ proteins in brain endothelial cells was often followed by their down-regulation and/or re-localization, leading to TJ destabilization and permeability increase [136-138,171].”
• Astrocyte-derived VEGF-A drives blood-brain barrier disruption in CNS inflammatory disease. (2012, background): “In spinal cords of controls at 21 dpi, typical pathology of EAE was observed, including astrogliosis (Figure 5C), BBB breakdown The Journal of Clinical Investigation http://www.jci.org Volume 122 Number 7 July 2012 2457 (Figure 5D), inflammatory cell infiltration (Figure 5E), and multifocal demyelin”
• The blood–brain barrier in health and disease: Important unanswered questions (2020, background): “Indeed, several molecular factors regulate BBB dysfunction in multiple diseases, including vascular endothelial growth factor (Argaw et al., 2009, 2012), inflammatory cytokines (tumor necrosis factor α [Nishioku et al., 2010], interleukins 1 and 6 [Chiaretti et al., 2005; Paré et al., 2018; Wang…”
• Blood-brain barrier pathophysiology in traumatic brain injury (2011, background): “The VEGFA-induced downregulation of expression of another tight junction protein CLDN5 in brain endothelial cell cultures was also reported, and the microinjection of VEGFA into a mouse cerebral cortex was shown to result in the disruption of normal pattern of immunostaining for occludin and CLDN5, ”
• Astrocytes: biology and pathology (2009, background): “2b) to gain of detrimental effects such as (1) exacerbating inflammation via cytokine production [22, 23], (2) producing neurotoxic levels of reactive oxygen species [92, 234], (3) releasing potentially excitotoxic glutamate [238], (4) potential contribution to seizure genesis [106, 240], (5) compro”
• Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “VEGF secretion by reactive astrocytes can serve as a good example of a context-dependent response: the positive, stimulatory effect of VEGF on the formation of vessels and synapses in ischemic stroke (20, 263) contrasts with its induction of blood-brain barrier breakdown and lymphocyte infiltration ”
• The blood-brain barrier. (2015, background): “Although VEGF is a factor mostly known to promote angiogenesis during development, in adulthood, VEGF decreases the stability of the BBB during inflammatory conditions (Argaw et al. 2009, 2012).”
• Astrocyte roles in traumatic brain injury (2015, background): “For example, in response to stimulation by the pro-inflammatory cytokine IL-β, astrocytes generate and release vasoactive endothelial growth factor (VEGF) that increases blood-brain barrier permeability and promotes leukocyte extravasation (Argaw et al., 2009; Argaw et al., 2012).”