ArticleJournal of neuroinflammation2014
Heat shock protein 60: an endogenous inducer of dopaminergic cell death in Parkinson disease.
Article in Journal of neuroinflammation, 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, 44 citations in OpenAlex.
- Aberrations in peripheral B lymphocytes and B lymphocyte subsets levels in Parkinson disease: a systematic review.Frontiers in immunology · 2025Pooled it
- Parkinson's disease neurons exhibit alterations in mitochondrial quality control proteins.NPJ Parkinson's disease · 2023Article
- The penalty of stress - Epichaperomes negatively reshaping the brain in neurodegenerative disorders.Journal of neurochemistry · 2021Review
- Heat shock proteins with an emphasis on HSP 60.Molecular biology reports · 2021Review
- HSP60 critically regulates endogenous IL-1β production in activated microglia by stimulating NLRP3 inflammasome pathway.Journal of neuroinflammation · 2018Article
- Mitochondrial Chaperones in the Brain: Safeguarding Brain Health and Metabolism?Frontiers in endocrinology · 2018Article
- Peripheral Lymphocyte Subsets as a Marker of Parkinson's Disease in a Chinese Population.Neuroscience bulletin · 2017Article
- Hydroxysafflor Yellow A Improves Motor Dysfunction in the Rotenone-Induced Mice Model of Parkinson's Disease.Neurochemical research · 2017Article
- Microfluidic Sample Preparation for Single Cell Analysis.Analytical chemistry · 2016Review
- e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease.Mediators of inflammation · 2016Article
- Effects of cordycepin on the microglia-overactivation-induced impairments of growth and development of hippocampal cultured neurons.PloS one · 2015Article
- Clinical characteristics and peripheral T cell subsets in Parkinson's disease patients with constipation.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreasing evidence suggests that inflammation associated with microglial cell activation in the substantia nigra (SN) of patients with Parkinson disease (PD) is not only a consequence of neuronal degeneration, but may actively sustain dopaminergic (DA) cell loss over time. We aimed to study whether the intracellular chaperone heat shock protein 60 (Hsp60) could serve as a signal of CNS injury for activation of microglial cells.
methodsHsp60 mRNA expression in the mesencephalon and the striatum of C57/BL6 mice treated with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and the Hsp60/TH mRNA ratios in the SN of PD patients and aged-matched subjects were measured. To further investigate a possible link between the neuronal Hsp60 response and PD-related cellular stress, Hsp60 immunoblot analysis and quantification in cell lysates from SH-SY5Y after treatment with 100 μM MPP+ (1-methyl-4-phenylpyridinium) at different time points (6, 12, 24 and 48 hours) compared to control cells were performed. Additional MTT and LDH assay were used. We next addressed the question as to whether Hsp60 influences the survival of TH+ neurons in mesencephalic neuron-glia cultures treated either with MPP+ (1 μM), hHsp60 (10 μg/ml) or a combination of both. Finally, we measured IL-1β, IL-6, TNF-α and NO-release by ELISA in primary microglial cell cultures following treatment with different hHsp60 preparations. Control cultures were exposed to LPS.
resultsIn the mesencephalon and striatum of mice treated with MPTP and also in the SN of PD patients, we found that Hsp60 mRNA was up-regulated. MPP+, the active metabolite of MPTP, also caused an increased expression and release of Hsp60 in the human dopaminergic cell line SH-SY5Y. Interestingly, in addition to being toxic to DA neurons in primary mesencephalic cultures, exogenous Hsp60 aggravated the effects of MPP+. Yet, although we demonstrated that Hsp60 specifically binds to microglial cells, it failed to stimulate the production of pro-inflammatory cytokines or NO by these cells.
conclusionsOverall, our data suggest that Hsp60 is likely to participate in DA cell death in PD but via a mechanism unrelated to cytokine release.
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