ArticleDrug design, development and therapy2019
Cathepsin G cleaves and activates IL-36γ and promotes the inflammation of psoriasis.
Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- IL-36-Driven Inflammation in Generalized Pustular Psoriasis: Immunological Insights from Plaque Psoriasis and Implications for Targeted Therapy.International journal of molecular sciences · 2026Review
- New Non-Saccharide Heparin Mimetics as Inhibitors of Cathepsin G.Chemical biology & drug design · 2026Article
- The IL-36 Cytokine Rheostat: Hierarchical Regulation of Epithelial-Immune Crosstalk and Precision Therapy in Psoriatic and Related Dermatoses.Clinical, cosmetic and investigational dermatology · 2026Review
- Drug repurposing of cyclin-dependent kinase inhibitors for neutrophilic acute respiratory distress syndrome and psoriasis.Journal of advanced research · 2025Review
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- Regulation of epidermal barrier function and pathogenesis of psoriasis by serine protease inhibitors.Frontiers in immunology · 2024Review
- NETosis of psoriasis: a critical step in amplifying the inflammatory response.Frontiers in immunology · 2024Review
- SerpinB3/B4 Abates Epithelial Cell-Derived CXCL8/IL-8 Expression in Chronic Rhinosinusitis with Nasal Polyps.Journal of immunology research · 2024Article
- Targeting IL-36 in Inflammatory Skin Diseases.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023Article
- Homogeneous, Synthetic, Non-Saccharide Glycosaminoglycan Mimetics as Potent Inhibitors of Human Cathepsin G.Biomolecules · 2023Article
- The Potential Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Cardiovascular System, Respiratory System and Skin.International journal of molecular sciences · 2022Review
- SerpinB7 deficiency contributes to development of psoriasis via calcium-mediated keratinocyte differentiation dysfunction.Cell death & disease · 2022Article
- SERPINA3C ameliorates adipose tissue inflammation through the Cathepsin G/Integrin/AKT pathway.Molecular metabolism · 2022Article
- Advances in the pathogenesis of psoriasis: from keratinocyte perspective.Cell death & disease · 2022Review
- Indoleamine 2,3-dioxygenase adjusts neutrophils recruitment and chemotaxis inInternational journal of ophthalmology · 2022Article
- Low-Density Granulocytes in Immune-Mediated Inflammatory Diseases.Journal of immunology research · 2022Review
- Neutrophil Extracellular Traps in Skin Diseases.Biomedicines · 2021Review
- The Inhibitory Effect of Noscapine on the In Vitro Cathepsin G-Induced Collagen Expression in Equine Endometrium.Life (Basel, Switzerland) · 2021Article
- Article
- Generalized Pustular Psoriasis: Divergence of Innate and Adaptive Immunity.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIL-36γ is considered to be a valuable biomarker in psoriatic patients, which is expressed as an inactive precursor that needs to be proteolytically processed and activated, and neutrophil-derived proteases seemed to be potent activating enzymes of IL-36γ.
objectivesThis study aims to investigate the activation of IL-36γ by cathepsin G (CG) and neutrophil elastase (NE). MATERIALS AND
methodsWe used inactive recombinant full-length (FL)-IL-36γ with different doses of NE or CG to stimulate HaCaT cells; neutrophil extracellular traps (NETs) were prepared to act on FL-IL-36γ and then stimulate HaCaT cells. Real-time quantitative PCR and ELISA were performed to detect CXCL-1 and CXCL-8 expression. We developed imiquimod-induced psoriasis-like mouse model to evaluate the effect of hypodermic injection of neutrophil-derived protease or its inhibitor. Histopathology and Western blotting were conducted for effect assessment.
resultsPurified CG cleaved and activated recombinant human FL-IL-36γ to promote CXCL-1 and CXCL-8 expression by human keratinocytes, and NETs activated FL-IL-36γ and the activation was inhibited by serpin A3. CG induced expression of a more truncated IL-36γ in psoriasiform lesion of mice and aggravated the psoriasis-like lesion induced by imiquimod, whereas recombinant serpin A3 alleviated the severity of the psoriasis-like mouse mode.
conclusionCG has the ability to cleave and activate IL-36γ and aggravate imiquimod-induced mouse psoriasiform lesion. Thus, CG-specific inhibitors might be promising therapeutic drugs for psoriasis.
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Registered trials
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.