ArticleProceedings of the National Academy of Sciences of the United States of America2017
Phosphorylation of αB-crystallin supports reactive astrogliosis in demyelination.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- Resistance-exercise-induced stress intervenes in TGF-β signaling by cooperatively downregulating nuclear αB-crystallin and SMAD4 in human skeletal muscle fibers.The FEBS journal · 2026Article
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- Sox9 regulation of hexokinase 1 controls neuroinflammatory astrocyte subtypes in a rat model of neuropathic pain.Nature communications · 2025Article
- Disorder with consequence: Phosphorylation sites in HSPB5 yield distinct structural outcomes.bioRxiv : the preprint server for biology · 2025Article
- Integrative assessment of RNA sequencing and in silico analysis to pinpoint mRNAs, lncRNAs, and circRNAs interactions with miRNAs underlying arsenic-induced neurotoxicity.BMC genomics · 2025Article
- Early functional and structural hippocampal impairment in a bilateral common carotid artery stenosis mouse model.Animal models and experimental medicine · 2025Article
- Phosphorylation of CRYAB induces a condensatopathy to worsen post-myocardial infarction left ventricular remodeling.The Journal of clinical investigation · 2025Article
- Neuroinflammation and neurodegeneration following traumatic brain injuries.Anatomical science international · 2025Review
- Astrocyte Activation and Drug Target in Pathophysiology of Multiple Sclerosis.Methods in molecular biology (Clifton, N.J.) · 2024Review
- Phosphorylation of αB-Crystallin Involves Interleukin-1β-Mediated Intracellular Retention in Retinal Müller Cells: A New Mechanism Underlying Fibrovascular Membrane Formation.Investigative ophthalmology & visual science · 2023Article
- Astrocyte Immune Functions and Glaucoma.International journal of molecular sciences · 2023Review
- Deletion ofFrontiers in pharmacology · 2023Article
- Mechanisms underlying the beneficial effects of physical exercise on multiple sclerosis: focus on immune cells.Frontiers in immunology · 2023Review
- Human Retinal Organoids Provide a Suitable Tool for Toxicological Investigations: A Comprehensive Validation Using Drugs and Compounds Affecting the Retina.Stem cells translational medicine · 2022Article
- Single nuclei RNA sequencing investigation of the Purkinje cell and glial changes in the cerebellum of transgenic Spinocerebellar ataxia type 1 mice.Frontiers in cellular neuroscience · 2022Article
- Attenuating vascular stenosis-induced astrogliosis preserves white matter integrity and cognitive function.Journal of neuroinflammation · 2021Article
- The engineered expression of secreted HSPB5-Fc in CHO cells exhibits cytoprotection in vitro.BMC biotechnology · 2021Article
- Article
- Multiple Sclerosis Biomarker Discoveries by Proteomics and Metabolomics Approaches.Biomarker insights · 2021Review
- CRYAB predicts clinical prognosis and is associated with immunocyte infiltration in colorectal cancer.PeerJ · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The small heat shock protein αB-crystallin (CRYAB) has been implicated in multiple sclerosis (MS) pathogenesis. Earlier studies have indicated that CRYAB inhibits inflammation and attenuates clinical disease when administered in the experimental autoimmune encephalomyelitis model of MS. In this study, we evaluated the role of CRYAB in primary demyelinating events. Using the cuprizone model of demyelination, a noninflammatory model that allows the analysis of glial responses in MS, we show that endogenous CRYAB expression is associated with increased severity of demyelination. Moreover, we demonstrate a strong correlation between the expression of CRYAB and the extent of reactive astrogliosis in demyelinating areas and in in vitro assays. In addition, we reveal that CRYAB is differentially phosphorylated in astrocytes in active demyelinating MS lesions, as well as in cuprizone-induced lesions, and that this phosphorylation is required for the reactive astrocyte response associated with demyelination. Furthermore, taking a proteomics approach to identify proteins that are bound by the phosphorylated forms of CRYAB in primary cultured astrocytes, we show that there is clear differential binding of protein targets due to the specific phosphorylation of CRYAB. Subsequent Ingenuity Pathway Analysis of these targets reveals implications for intracellular pathways and biological processes that could be affected by these modifications. Together, these findings demonstrate that astrocytes play a pivotal role in demyelination, making them a potential target for therapeutic intervention, and that phosphorylation of CRYAB is a key factor supporting the pathogenic response of astrocytes to oligodendrocyte injury.
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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.