ArticleJournal of photochemistry and photobiology. B, Biology2013
UVA causes dual inactivation of cathepsin B and L underlying lysosomal dysfunction in human dermal fibroblasts.
Article in Journal of photochemistry and photobiology. B, Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 44 citations in OpenAlex.
- The Effects of Lipid Extracts from MicroalgaeAntioxidants (Basel, Switzerland) · 2025Article
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Spatiotemporal roles of AMPK in PARP-1- and autophagy-dependent retinal pigment epithelial cell death caused by UVA.Journal of biomedical science · 2023Article
- The Mechanism of Peach Gum Polysaccharide Preventing UVB-Induced Skin Photoaging by Regulating Matrix Metalloproteinanse and Oxidative Factors.Molecules (Basel, Switzerland) · 2023Article
- Autophagy plays an essential role in ultraviolet radiation-driven skin photoaging.Frontiers in pharmacology · 2022Review
- The Endogenous Tryptophan-derived Photoproduct 6-formylindolo[3,2-b]carbazole (FICZ) is a Nanomolar Photosensitizer that Can be Harnessed for the Photodynamic Elimination of Skin Cancer Cells in Vitro and in Vivo.Photochemistry and photobiology · 2021Article
- Circular RNA expression profiles significantly altered in UVA-irradiated human dermal fibroblasts.Experimental and therapeutic medicine · 2020Article
- Alterations in extracellular matrix composition during aging and photoaging of the skin.Matrix biology plus · 2020Article
- Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects ofAntioxidants (Basel, Switzerland) · 2020Article
- Photoprotective effect of Astragalus membranaceus polysaccharide on UVA-induced damage in HaCaT cells.PloS one · 2020Article
- Protective Effects and Mechanisms ofInternational journal of molecular sciences · 2019Article
- Autophagic Control of Skin Aging.Frontiers in cell and developmental biology · 2019Review
- Mechanistic insights into environmental and genetic risk factors for systemic lupus erythematosus.American journal of translational research · 2019Review
- The BPhotochemistry and photobiology · 2017Article
- Parkinson's Disease Skin Fibroblasts Display Signature Alterations in Growth, Redox Homeostasis, Mitochondrial Function, and Autophagy.Frontiers in neuroscience · 2017Article
- Ultraviolet A Enhances Cathepsin L Expression and Activity via JNK Pathway in Human Dermal Fibroblasts.Chinese medical journal · 2016Article
- Article
- The Nrf2-inducers tanshinone I and dihydrotanshinone protect human skin cells and reconstructed human skin against solar simulated UV.Redox biology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cutaneous exposure to chronic solar UVA-radiation is a causative factor in photocarcinogenesis and photoaging. Recently, we have identified the thiol-dependent cysteine-protease cathepsin B as a novel UVA-target undergoing photo-oxidative inactivation upstream of autophagic-lysosomal dysfunction in fibroblasts. In this study, we examined UVA effects on a wider range of cathepsins and explored the occurrence of UVA-induced cathepsin inactivation in other cultured skin cell types. In dermal fibroblasts, chronic exposure to non-cytotoxic doses of UVA caused pronounced inactivation of the lysosomal cysteine-proteases cathepsin B and L, effects not observed in primary keratinocytes and occurring only to a minor extent in primary melanocytes. In order to determine if UVA-induced lysosomal impairment requires single or dual inactivation of cathepsin B and/or L, we used a genetic approach (siRNA) to selectively downregulate enzymatic activity of these target cathepsins. Monitoring an established set of protein markers (including LAMP1, LC3-II, and p62) and cell ultrastructural changes detected by electron microscopy, we observed that only dual genetic antagonism (targeting both CTSB and CTSL expression) could mimic UVA-induced autophagic-lysosomal alterations, whereas single knockdown (targeting CTSB or CTSL only) did not display 'UVA-mimetic' effects failing to reproduce the UVA-induced phenotype. Taken together, our data demonstrate that chronic UVA inhibits both cathepsin B and L enzymatic activity and that dual inactivation of both enzymes is a causative factor underlying UVA-induced impairment of lysosomal function in dermal fibroblasts.
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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.