MAP kinase pathways in UV-induced apoptosis of retinal pigment epithelium ARPE19 cells
Open accessAbstract
The retinal pigment epithelium (RPE) is constantly exposed to external injuries which lead to degeneration, dysfunction or loss of RPE cells. The balance between RPE cells death and proliferation may be responsible for several diseases of the underlying retina, including age-related macular degeneration (AMD) and proliferative vitreoretinopathy (PVR). Signaling pathways able to control cells proliferation or death usually involve the MAPK (mitogen-activated protein kinases) pathways, which modulate the activity of transcription factors by phosphorylation. UV exposure induces DNA breakdown and causes cellular damage through the production of reactive oxygen species (ROS) leading to programmed cell death. In this study, human retinal pigment epithelial cells ARPE19 were exposed to 100 J/m(2) of UV-C and MAPK pathways were studied. We first showed the expression of the three major MAPK pathways. Then we showed that activator protein-1 (AP-1) was activated through phosphorylation of cJun and cFos, induced by JNK and p38, respectively. Specific inhibitors of both kinases decreased their respective activities and phosphorylation of their nuclear targets (cJun and cFos) and reduced UV-induced cell death. The use of specific kinases inhibitors may provide excellent tools to prevent RPE apoptosis specifically in RPE diseases involving ROS and other stress-related compounds such as in AMD.
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ERK1/2 activity is decreased when ARPE19 cells are exposed to UV stress.
“is decreased when ARPE19 cells are exposed to UV stress”
From Loss of Extracellular Signal-Regulated Kinase 1/2 in the Retinal Pigment Epithelium Leads to RPE65 Decrease and Retinal Degeneration (2017) · cites this paper as [24]
The Discussion reports a slight decrease in phospho-ERK1/2 in ARPE19 cells after UV stress. The Results also report decreased ERK2 phosphorylation, but say that an assay to measure ERK2 activity was unavailable. The phosphorylation finding supports the direction of the claim, but the paper did not directly establish decreased ERK1/2 activity. (LLM, conf=0.85)
Experimental — accuracy not yet measuredOxidative stress activates MAPK components ERK, JNK, and p38, which contribute to RPE cell apoptosis, inflammatory responses, and pathological angiogenesis.
“Oxidative stress, a key driver of AMD, activates MAPK components-including ERK, JNK, and p38-which contribute to retinal pigment epithelium (RPE) cell apoptosis, inflammatory responses, and pathological angiogenesis 16,17,37,38 .”
From rAAV-mediated Multi-miRNA Delivery Targeting MAPK Pathway Suppresses Laser-induced Choroidal Neovascularization in Mice (2026) · cites this paper as [16]
The Introduction links oxidative stress to JNK and p38 signaling, and the Abstract reports that inhibiting those kinases reduced UV-induced apoptosis in ARPE19 cells. The Discussion instead reports a slight decrease in ERK1/2 activation after UV exposure and suggests ERK1/2 may be anti-apoptotic in this model. The Introduction discusses inflammatory responses generally, but the paper does not establish RPE inflammation or pathological angiogenesis as outcomes of these pathways. Page numbers were not provided in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredUV-C irradiation of RPE cells induces cell death through the activation of both JNK and p38 that is reversed by the use of specific kinase inhibitors, namely, D-JNKi and SB203580.
“UV-C irradiation of RPE cells induces cell death through the activation of both JNK and p38 that is reversed by the use of specific kinase inhibitors, namely, D-JNKi and SB203580 [ 38 ].”
From MAPK Pathways in Ocular Pathophysiology: Potential Therapeutic Drugs and Challenges (2023) · cites this paper as [38]
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References 50 · Cited by 110
- Authors
- Roduit, R., & Schorderet, D. F.
- Affiliations
- Institut de Recherche en Opthalmologie (CH)
- Corresponding author
- Roduit, Raphaël
- Venue
- Apoptosis
- Published
- 2008-02-06
- Volume
- 13
- Issue
- 3
- Pages
- 343-353
- ISSN
- 1360-8185 (ISSN-L)
- 1573-675X
- OpenAlex
- W2106868003
- Cited by
- 110
- References
- 50
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 3 · 2020: 5 · 2019: 6 · 2018: 12 · 2017: 7 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 14 · 2012: 5
- FWCI
- 8.43
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- APOPTOSIS (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (publishedVersion, other-oa)
- reroDoc Digital Library (submittedVersion)
- IRIS (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- MAPK signaling, UV-induced apoptosis, retinal pigment epithelium, ARPE-19 cells, age-related macular degeneration, proliferative vitreoretinopathy, JNK, p38 MAPK, activator protein-1, c-Jun, c-fos, reactive oxygen species, kinase inhibitors
- MeSH terms
- Cell Line, Humans, Pigment Epithelium of Eye, Retina, Ultraviolet Rays, Proto-Oncogene Proteins c-fos, Apoptosis, Transcription Factor AP-1, Mitogen-Activated Protein Kinase 1, MAP Kinase Signaling System, p38 Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 8, Mitogen-Activated Protein Kinase 9, MAP Kinase Kinase 4
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