ArticleFluids and barriers of the CNS2014
Increased blood-brain barrier permeability and alterations in perivascular astrocytes and pericytes induced by intracisternal glutaric acid.
Article in Fluids and barriers of the CNS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Laminin as a Biomarker of Blood-Brain Barrier Disruption under Neuroinflammation: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Odd-Chain Dicarboxylic Acid Feeding Produces a Glutaric Aciduria Type 1-Like Metabolic Signature in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Article
- Tetramethylpyrazine promotes stroke recovery by inducing the restoration of neurovascular unit and transformation of A1/A2 reactive astrocytes.Frontiers in cellular neuroscience · 2023Article
- Gestational and Lactational Iron Deficiency Anemia Impairs Myelination and the Neurovascular Unit in Infant Rats.Molecular neurobiology · 2022Article
- Neuroprotective effects of violacein in a model of inherited amyotrophic lateral sclerosis.Scientific reports · 2022Article
- The pathogenic role of c-Kit+ mast cells in the spinal motor neuron-vascular niche in ALS.Acta neuropathologica communications · 2021Article
- Glutaric Acid Affects Pericyte Contractility and Migration: Possible Implications for GA-I Pathogenesis.Molecular neurobiology · 2019Article
- Neurological manifestations of organic acidurias.Nature reviews. Neurology · 2019Review
- Targeting pericytes for neurovascular regeneration.Cell communication and signaling : CCS · 2019Review
- Stem Cells as a Promising Tool for the Restoration of Brain Neurovascular Unit and Angiogenic Orientation.Molecular neurobiology · 2017Review
- Higher Vulnerability of Menadione-Exposed Cortical Astrocytes of Glutaryl-CoA Dehydrogenase Deficient Mice to Oxidative Stress, Mitochondrial Dysfunction, and Cell Death: Implications for the Neurodegeneration in Glutaric Aciduria Type I.Molecular neurobiology · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundGlutaric acid (GA) is a dicarboxylic acid that accumulates in millimolar concentrations in glutaric acidemia I (GA-I), an inherited neurometabolic childhood disease characterized by extensive neurodegeneration. Vascular dysfunction is a common and early pathological feature in GA-I, although the underlying mechanisms remain unknown. In the present study, we have used a previously-validated rat model of GA-I to determine the effect of GA on the blood- brain barrier (BBB) and the neurovascular unit.
methodsNewborn rat pups received a single injection of GA (1 μmol/g) or vehicle into the cisterna magna. BBB permeability was analyzed at 14 and 30 days post injection (DPI) by assessing Evans blue (EB) and immunoglobulin G (IgG) extravasation. Blood vessels and microglia were labeled with tomato lectin. Characterization of EB positive cells was made by double labeling with antibodies to astrocyte and neuronal markers. Immunohistochemistry against aquaporin 4 (AQP4), β receptor of the platelet derived growth factor (PDGFRβ) and laminin was used to recognize astrocyte endfeet, pericytes and basal lamina. Zonula occludens 1 (ZO-1) and occludin striatal expression was assessed by Western blotting.
resultsPerinatal intracisternal GA administration caused an increased extravasation of free EB, but not of IgG, into the striatal parenchyma at 14 and 30 DPI. EB extravasated through the BBB was internalized exclusively into neurons. GA-injected animals did not show significant changes in the area of small blood vessels in the striatum, but at 30 DPI there was a significant decrease in AQP4, PDGFRβ and laminin positive areas associated with small blood vessels. Occludin and ZO-1 expression in the striatal tissue was unchanged in all conditions analyzed.
conclusionsThe present study shows a previously-unknown effect of a perinatal administration of a single intracisternal GA injection on BBB permeability and on key components of the neurovascular unit. The results suggest BBB leakage is a pathogenic mechanism and a potential therapeutic target for patients with GA-I.
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