ArticleMetabolic brain disease2006
Propionic acid induces cytoskeletal alterations in cultured astrocytes from rat cerebral cortex.
Article in Metabolic brain disease, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Metabolic toxicity and neurological dysfunction in methylmalonic acidemia: from mechanisms to therapeutics.Molecular medicine (Cambridge, Mass.) · 2025Review
- Elevated propionate and its association with neurological dysfunctions in propionic acidemia.Frontiers in molecular neuroscience · 2025Review
- Pathophysiological mechanisms of complications associated with propionic acidemia.Pharmacology & therapeutics · 2023Review
- Dietary Fiber Modulates the Release of Gut Bacterial Products Preventing Cognitive Decline in an Alzheimer's Mouse Model.Cellular and molecular neurobiology · 2023Article
- The Intervention of Prebiotics on Depression via the Gut-Brain Axis.Molecules (Basel, Switzerland) · 2022Review
- Shedding light on biological sex differences and microbiota-gut-brain axis: a comprehensive review of its roles in neuropsychiatric disorders.Biology of sex differences · 2022Review
- The anti-inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters.Food science & nutrition · 2021Article
- The Neuroprotective Effect of Tea Polyphenols on the Regulation of Intestinal Flora.Molecules (Basel, Switzerland) · 2021Review
- Gut microbial metabolites in depression: understanding the biochemical mechanisms.Microbial cell (Graz, Austria) · 2019Review
- The Microbiota-Gut-Brain Axis in Neuropsychiatric Disorders: Pathophysiological Mechanisms and Novel Treatments.Current neuropharmacology · 2018Article
- "Classical organic acidurias": diagnosis and pathogenesis.Clinical and experimental medicine · 2017Review
- May the Force Be With You: The Light and Dark Sides of the Microbiota-Gut-Brain Axis in Neuropsychiatry.CNS drugs · 2016Review
- Gene expression in cell lines from propionic acidemia patients, carrier parents, and controls.Molecular genetics and metabolism · 2015Article
- Signaling mechanisms and disrupted cytoskeleton in the diphenyl ditelluride neurotoxicity.Oxidative medicine and cellular longevity · 2014Review
- Cytoskeleton as a potential target in the neuropathology of maple syrup urine disease: insight from animal studies.Journal of inherited metabolic disease · 2007Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe neurological symptoms, cerebral edema, and atrophy are common features of the inherited metabolic disorder propionic acidemia. However, the pathomechanisms involved in the neuropathology of this disease are not well established. In this study, we investigate the effects of propionic acid (PA), a metabolite accumulating in this disorder, on cytoskeletal reorganization, on cell viability, and on the in vitro phosphorylation of glial fibrillary acidic protein (GFAP) and vimentin in cultured astrocytes from cerebral cortex of neonatal rats. We observed that the astrocytes changed their usual polygonal morphology when exposed to 5 mM PA for 72 h, leading to the appearance of fusiform or process-bearing cells, without elicit cell death. We also noticed that after 72 h treatment with 5 mM PA cells showed retracted cytoplasm with bipolar processes containing packed GFAP filaments and disorganized actin stress fibers, as revealed by immunocytochemistry. In addition, the morphological alterations were accompanied by increased in vitro 32P incorporation into GFAP and vimentin recovered into the high-salt Triton-insoluble cytoskeletal fraction. In conclusion, our results indicate that PA lead to cytoskeletal reorganization and to increased in vitro phosphorylation of Triton-insoluble GFAP and vimentin. On the basis of our results we could suppose that Triton-insoluble GFAP and vimentin hyperphosphorylation could be implicated in the reorganization of cellular structure and these findings could be involved in the brain damage characteristic of propionic acidemia patients.
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