ArticleHuman molecular genetics2016
αB-Crystallin overexpression in astrocytes modulates the phenotype of the BACHD mouse model of Huntington's disease.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Single-cell transcriptomics of human brain disorders.Molecular psychiatry · 2026Review
- Multi-omic analysis of Huntington's disease reveals a compensatory astrocyte state.Nature communications · 2024Article
- Reactive astrocytes secrete the chaperone HSPB1 to mediate neuroprotection.Science advances · 2024Article
- Regulation of rat HspB5/alphaB-Crystallin by microRNAs miR-101a-3p, miR-140-5p, miR-330-5p, and miR-376b-3p.Cell stress & chaperones · 2023Article
- Multi-OMIC analysis of Huntington disease reveals a neuroprotective astrocyte state.bioRxiv : the preprint server for biology · 2023Article
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- The Role of Small Heat Shock Proteins in Protein Misfolding Associated Motoneuron Diseases.International journal of molecular sciences · 2022Review
- Modifier pathways in polyglutamine (PolyQ) diseases: from genetic screens to drug targets.Cellular and molecular life sciences : CMLS · 2022Review
- Alpha B-Crystallin in Muscle Disease Prevention: The Role of Physical Activity.Molecules (Basel, Switzerland) · 2022Review
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- Insights on Human Small Heat Shock Proteins and Their Alterations in Diseases.Frontiers in molecular biosciences · 2022Review
- Antibody and Protein Profiles in Glaucoma: Screening of Biomarkers and Identification of Signaling Pathways.Biology · 2021Review
- The engineered expression of secreted HSPB5-Fc in CHO cells exhibits cytoprotection in vitro.BMC biotechnology · 2021Article
- AlphaB-crystallin and breast cancer: role and possible therapeutic strategies.Cell stress & chaperones · 2021Review
- Small heat shock proteins in neurodegenerative diseases.Cell stress & chaperones · 2020Review
- Differentiation Drives Widespread Rewiring of the Neural Stem Cell Chaperone Network.Molecular cell · 2020Article
- The noncanonical small heat shock protein HSP-17 fromThe Journal of biological chemistry · 2020Article
- Rapidly progressive amyotrophic lateral sclerosis is associated with microglial reactivity and small heat shock protein expression in reactive astrocytes.Neuropathology and applied neurobiology · 2019Article
- XBP1 signalling is essential for alleviating mutant protein aggregation in ER-stress related skeletal disease.PLoS genetics · 2019Article
- Mutant huntingtin reduction in astrocytes slows disease progression in the BACHD conditional Huntington's disease mouse model.Human molecular genetics · 2019Article
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Authors and funding
5 authors at 4 institutions in 4 countries.
Funding
Abstract
Huntington's disease (HD) is caused by an expanded polyglutamine (polyQ) tract in the huntingtin (htt) protein. The polyQ expansion increases the propensity of htt to aggregate and accumulate, and manipulations that mitigate protein misfolding or facilitate the clearance of misfolded proteins are predicted to slow disease progression in HD models. αB-crystallin (αBc) or HspB5 is a well-characterized member of the small heat shock protein (sHsp) family that reduces mutant htt (mhtt) aggregation and toxicity in vitro and in Drosophila models of HD. Here, we determined if overexpressing αBc in vivo modulates aggregation and delays the onset and progression of disease in a full-length model of HD, BACHD mice. Expression of sHsps in neurodegenerative disease predominantly occurs in non-neuronal cells, and in the brain, αBc is mainly found in astrocytes and oligodendrocytes. Here, we show that directed αBc overexpression in astrocytes improves motor performance in rotarod and balance beam tests and improves cognitive function in the BACHD mice. Improvement in behavioral deficits correlated with mitigation of neuropathological features commonly observed in HD. Interestingly, astrocytic αBc overexpression was neuroprotective against neuronal cell loss in BACHD brains, suggesting αBc might be acting in a non-cell-autonomous manner. At the protein level, αBc decreased the level of soluble mhtt and decreased the size of mhtt inclusions in BACHD brain. Our results support a model in which elevating astrocytic αBc confers neuroprotection through a potential non-cell-autonomous pathway that modulates mhtt aggregation and protein levels.
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