ArticlePloS one2013
Cathepsin B is up-regulated and mediates extracellular matrix degradation in trabecular meshwork cells following phagocytic challenge.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Amanitin-Based Fc-Small Molecule-Drug Conjugates with Noncleavable Linker: A Novel Therapeutic Strategy for Prostate Cancer Targeted Therapy.Molecular cancer therapeutics · 2026Article
- Muscle Cathepsin B Treatment Improves Behavioral and Neurogenic Deficits in a Mouse Model of Alzheimer's Disease.Aging cell · 2025Article
- Measurements of Phagocytosis in Trabecular Meshwork Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Glaucoma: Novel antifibrotic therapeutics for the trabecular meshwork.European journal of pharmacology · 2023Review
- B cell peripheral tolerance is promoted by cathepsin B protease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Type I Cystatin Derived fromPathogens (Basel, Switzerland) · 2023Article
- Role of TFEB in Diseases Associated with Lysosomal Dysfunction.Advances in experimental medicine and biology · 2023Article
- Circulating monocytes associated with anti-PD-1 resistance in human biliary cancer induce T cell paralysis.Cell reports · 2022Article
- Molecular Features of CA-074 pH-Dependent Inhibition of Cathepsin B.Biochemistry · 2022Article
- Role of NLRP3 Inflammasome in Myocardial Ischemia-Reperfusion Injury and Ventricular Remodeling.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- Quantitative proteomic analysis reveals the molecular mechanism of the Yesso scallop (Computational and structural biotechnology journal · 2022Article
- Deficiency in Lyst function leads to accumulation of secreted proteases and reduced retinal adhesion.PloS one · 2022Article
- Article
- Relevant mediators involved in and therapies targeting the inflammatory response induced by activation of the NLRP3 inflammasome in ischemic stroke.Journal of neuroinflammation · 2021Review
- Review
- Cathepsins in neuronal plasticity.Neural regeneration research · 2021Article
- Cathepsin B Localizes in the Caveolae and Participates in the Proteolytic Cascade in Trabecular Meshwork Cells. Potential New Drug Target for the Treatment of Glaucoma.Journal of clinical medicine · 2020Article
- Review
- Betalain exerts a protective effect against glaucoma is majorly through the association of inflammatory cytokines.AMB Express · 2020Article
- A novel cystatin derived from Trichinella spiralis suppresses macrophage-mediated inflammatory responses.PLoS neglected tropical diseases · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cells in the trabecular meshwork (TM), a tissue responsible for draining aqueous humor out of the eye, are known to be highly phagocytic. Phagocytic activity in TM cells is thought to play an important role in outflow pathway physiology. However, the molecular mechanisms triggered by phagocytosis in TM cells are unknown. Here we investigated the effects of chronic phagocytic stress on lysosomal function using different phagocytic ligands (E. coli, carboxylated beads, collagen I-coated beads, and pigment). Lysotracker red co-localization and electron micrographs showed the maturation of E. coli- and collagen I-coated beads-containing phagosomes into phagolysosomes. Maturation of phagosomes into phagolysosomes was not observed with carboxylated beads or pigment particles. In addition, phagocytosis of E. coli and collagen I-coated beads led to increased lysosomal mass, and the specific up-regulation and activity of cathepsin B (CTSB). Higher levels of membrane-bound and secreted CTSB were also detected. Moreover, in vivo zymography showed the intralysosomal degradation of ECM components associated with active CTSB, as well as an overall increased gelatinolytic activity in phagocytically challenged TM cells. This increased gelatinolytic activity with phagocytosis was partially blocked with an intracellular CTSB inhibitor. Altogether, these results suggest a potential role of phagocytosis in outflow pathway tissue homeostasis through the up-regulation and/or proteolytic activation of extracellular matrix remodeling genes.
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