ReviewFrontiers in cellular neuroscience2015
The Role of Stefin B in Neuro-inflammation.
Review in Frontiers in cellular neuroscience, 2015. 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, 34 citations in OpenAlex.
- Article
- Article
- Stefin B alleviates the gouty arthritis in mice by inducing the M2 polarization of macrophages.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- CSTB gene replacement improves neuroinflammation, neurodegeneration and ataxia in murine type 1 progressive myoclonus epilepsy.Gene therapy · 2024Article
- Review
- Article
- Cathepsin B abundance, activity and microglial localisation in Alzheimer's disease-Down syndrome and early onset Alzheimer's disease; the role of elevated cystatin B.Acta neuropathologica communications · 2023Article
- Human stefin B: from its structure, folding, and aggregation to its function in health and disease.Frontiers in molecular neuroscience · 2022Review
- Association between Cardiorespiratory Fitness and Circulating Proteins in 50-Year-Old Swedish Men and Women: a Cross-Sectional Study.Sports medicine - open · 2021Article
- Altered Expression of Peroxiredoxins in Mouse Model of Progressive Myoclonus Epilepsy upon LPS-Induced Neuroinflammation.Antioxidants (Basel, Switzerland) · 2021Article
- Neuroinflammation and progressive myoclonus epilepsies: from basic science to therapeutic opportunities.Expert reviews in molecular medicine · 2020Review
- Parasite Cystatin: Immunomodulatory Molecule with Therapeutic Activity against Immune Mediated Disorders.Pathogens (Basel, Switzerland) · 2020Review
- RP-HPLC-ESI-IT Mass Spectrometry Reveals Significant Variations of the Human Salivary Protein Profile Associated with Predominantly Antibody Deficiencies.Journal of clinical immunology · 2020Article
- Proximal Tubule Translational Profiling during Kidney Fibrosis Reveals Proinflammatory and Long Noncoding RNA Expression Patterns with Sexual Dimorphism.Journal of the American Society of Nephrology : JASN · 2020Article
- The human olfactory cleft mucus proteome and its age-related changes.Scientific reports · 2018Article
- Journey of cystatins from being mere thiol protease inhibitors to at heart of many pathological conditions.International journal of biological macromolecules · 2017Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stefin B (cystatin B) is an endogenous cysteine cathepsin inhibitor localized in the cytosol, mitochondria and nucleus. Its expression is upregulated upon macrophage activation and cellular stress. Mutations in the gene of stefin B are associated with the neurodegenerative disease known as Unverricht-Lundborg disease (EPM1). It was reported that early microglial activation precedes neuronal loss in the brain of the stefin B-deficient mice, implying a role of the inhibitor at the cross-talk between microglia and cerebellar cells. Detailed analysis of microglial activation in stefin B-deficient microglia showed a significantly higher proportion of both pro-inflammatory M1 and anti-inflammatory M2 microglia in stefin B-deficient mouse brain compared with control mice. In our recent work, we demonstrated that stefin B-deficient mice were significantly more sensitive to the lethal lipopolysaccharide (LPS)-induced sepsis, due to increased caspase-11 expression and secreted higher amounts of pro-inflammatory cytokines IL-1β and IL-18. Upon LPS stimulation, stefin B was targeted into the mitochondria, and the lack of stefin B resulted in the increased destabilization of the mitochondrial membrane potential and mitochondrial superoxide generation. The increased caspase-11 gene expression and better pro- inflammatory caspase-1 and -11 activation determined in stefin B deficient bone marrow-derived macrophages resulted in enhanced non-canonical inflammasome activation. Since signaling pathways in macrophages could be compared to the ones in microglia we propose that inflammasome activation could play an important role in the pathogenesis of EPM1.
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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.