ArticleJournal of the American Society of Nephrology : JASN2017
Osmotic Stress-Induced Defective Glial Proteostasis Contributes to Brain Demyelination after Hyponatremia Treatment.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 50 citations in OpenAlex.
- Managing hyponatremia: fast or slow? Why, when, how, and controversies.Clinical kidney journal · 2026Review
- Effect of experimental hypoosmolar hyponatremia on the blood brain barrier and brain edema formation.Scientific reports · 2025Article
- The link between gut microbiota and multiple sclerosis from the perspective of barrier function.Frontiers in immunology · 2025Review
- The ubiquitin codes in cellular stress responses.Protein & cell · 2024Review
- Thalamic Neuron Resilience during Osmotic Demyelination Syndrome (ODS) Is Revealed by Primary Cilium Outgrowth and ADP-ribosylation factor-like protein 13B Labeling in Axon Initial Segment.International journal of molecular sciences · 2023Article
- Adaptation of the Brain to Hyponatremia and Its Clinical Implications.Journal of clinical medicine · 2023Review
- Review
- Cas9-mediated genome editing reveals a significant contribution of calcium signaling pathways to anhydrobiosis in Pv11 cells.Scientific reports · 2021Article
- Osmotic demyelination syndrome following slow correction of hyponatraemia.BMJ case reports · 2021Article
- Central pontine myelinolysis and the osmotic demyelination syndromes: an open and shut case?Acta neurologica Belgica · 2021Review
- Effective treatment of osmotic demyelination syndrome with plasmapheresis: a case report and review of the literature.Journal of medical case reports · 2021Review
- Endocytic regulation of cellular ion homeostasis controls lysosome biogenesis.Nature cell biology · 2020Article
- Review
- Nimodipine-Dependent Protection of Schwann Cells, Astrocytes and Neuronal Cells from Osmotic, Oxidative and Heat Stress Is Associated with the Activation of AKT and CREB.International journal of molecular sciences · 2019Article
- Ultrastructural Analysis of Thalamus Damages in a Mouse Model of Osmotic-Induced Demyelination.Neurotoxicity research · 2019Article
- Osmotic Demyelination: From an Oligodendrocyte to an Astrocyte Perspective.International journal of molecular sciences · 2019Review
- α-synuclein expression from a single copy transgene increases sensitivity to stress and accelerates neuronal loss in genetic models of Parkinson's disease.Experimental neurology · 2018Article
- Treatment of Severe Hyponatremia.Clinical journal of the American Society of Nephrology : CJASN · 2018Review
- Astroglial Modulation of Hydromineral Balance and Cerebral Edema.Frontiers in molecular neuroscience · 2018Review
- Hyponatremia and the Brain.Kidney international reports · 2018Review
Corrections and comments
- Commented on by
- Erratum issuedErratum.2017
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adequate protein folding is necessary for normal cell function and a tightly regulated process that requires proper intracellular ionic strength. In many cell types, imbalance between protein synthesis and degradation can induce endoplasmic reticulum (ER) stress, which if sustained, can in turn lead to cell death. In nematodes, osmotic stress induces massive protein aggregation coupled with unfolded protein response and ER stress. In clinical practice, patients sustaining rapid correction of chronic hyponatremia are at risk of osmotic demyelination syndrome. The intense osmotic stress sustained by brain cells is believed to be the major risk factor for demyelination resulting from astrocyte death, which leads to microglial activation, blood-brain barrier opening, and later, myelin damage. Here, using a rat model of osmotic demyelination, we showed that rapid correction of chronic hyponatremia induces severe alterations in proteostasis characterized by diffuse protein aggregation and ubiquitination. Abrupt correction of hyponatremia resulted in vigorous activation of both the unfolded protein response and ER stress accompanied by increased autophagic activity and apoptosis. Immunofluorescence revealed that most of these processes occurred in astrocytes within regions previously shown to be demyelinated in later stages of this syndrome. These results identify osmotic stress as a potent protein aggregation stimuli in mammalian brain and further suggest that osmotic demyelination might be a consequence of proteostasis failure on severe osmotic stress.
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