ArticleJournal of cellular and molecular medicine2011
Cathepsins and their endogenous inhibitors cystatins: expression and modulation in multiple sclerosis.
Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Cystatin C and its Role in the Neuro-Glial-Vascular Unit: Implications for Cerebrovascular Diseases and Neurodegeneration.Neuroscience bulletin · 2026Review
- Safety and efficacy of AAV8-aflibercept in treating choroidal neovascularization via single-cell RNA sequencing.Molecular therapy. Methods & clinical development · 2025Article
- Proteomic analysis of cerebrospinal fluid from females with multiple sclerosis highlights elevated microglial function and impaired neurogenesis.IBRO neuroscience reports · 2025Article
- The pH-Dependent Specificity of Cathepsin S and Its Implications for Inflammatory Communications and Disease.Biochemistry · 2025Article
- Cathepsins in Neurological Diseases.International journal of molecular sciences · 2025Review
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- Minoxidil and nebivolol restore aortic elastic fiber homeostasis in diabetic mice via potassium channel activation.Frontiers in physiology · 2025Article
- Proteogenomic analysis of human cerebrospinal fluid identifies neurologically relevant regulation and implicates causal proteins for Alzheimer's disease.Nature genetics · 2024Article
- Discovering Root Causal Genes with High Throughput Perturbations.bioRxiv : the preprint server for biology · 2024Article
- The Role of Cysteine Protease Cathepsins B, H, C, and X/Z in Neurodegenerative Diseases and Cancer.International journal of molecular sciences · 2023Review
- Proteogenomic analysis of human cerebrospinal fluid identifies neurologically relevant regulation and informs causal proteins for Alzheimer's disease.Research square · 2023Article
- Differential regulation of microglial states by colony stimulating factors.Frontiers in cellular neuroscience · 2023Review
- Tick innate immune responses to hematophagy andFrontiers in immunology · 2023Article
- Lysosomal peptidases-intriguing roles in cancer progression and neurodegeneration.FEBS open bio · 2022Review
- Mucopolysaccharidosis Type IVA: Extracellular Matrix Biomarkers in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022Article
- Transcriptomic Analysis of Peripheral Monocytes upon Fingolimod Treatment in Relapsing Remitting Multiple Sclerosis Patients.Molecular neurobiology · 2021Article
- Pharmacogenetic Predictors of Response to Interferon Beta Therapy in Multiple Sclerosis.Molecular neurobiology · 2021Article
- Cuprizone and EAE mouse frontal cortex proteomics revealed proteins altered in multiple sclerosis.Scientific reports · 2021Article
- The conserved autoimmune-disease risk geneProceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cathepsins are involved in a variety of physiological processes including antigen processing and presentation and extracellular matrix degradation. In the present study, we evaluated whether expression levels of cathepsins S and B and their inhibitors cystatins B and C are affected by multiple sclerosis (MS) disease state (relapse and remission) and therapies (interferon-β [IFN-β] and the glucocorticoid [GC] methylprednisolone), and whether they are associated with the IFN-β response phenotype. Real-time PCR was employed to compare RNA expression levels in peripheral blood leucocytes (PBLs) and ELISA to determine serum protein levels of MS patients and matched healthy individuals. Cathepsin S RNA was higher in MS patients in the relapse state compared to controls (by 74%, P = 3 × 10(-5), n = 30 versus n = 18) with a similar increase observed in serum (66%, P = 0.002, n = 18 versus n = 20). GC treatment reduced cathepsin S levels in PBL RNA (by 44%, P = 6 × 10(-6), n = 27) and serum proteins (by 27%, P = 1 × 10(-5), n = 26), reduced the serum protein levels of pro-cathepsin B (by 8%, P = 0.0007, n = 23), and in parallel increased the serum levels of their inhibitor cystatin C (by 82%, P = 8 × 10(-6), n = 26). IFN-β therapy significantly elevated the RNA levels (n = 16) of cathepsin B (by 16%, P = 0.03), cystatin B (44%, P = 0.004) and cystatin C (48%, P = 0.011). In the serum, only cathepsin S levels were reduced by IFN-β (16%, P = 0.006, n = 25). Interestingly, pre-treatment serum cathepsin S/cystatin C ratio was higher in 'good responders' to IFN-β therapy compared to patients without a good response (by 94%, P = 0.003). These results suggest that cathepsin S and cystatin C may contribute to disease activity in MS, specifically in a subgroup of patients that are responsive to IFN-β therapy, and that these proteins should be further evaluated as biomarkers in MS.
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