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Cited by 29Retinal Diseases and TreatmentsProtein Kinase Regulation and GTPase SignalingRetinal Development and Disorders

The DOI matches its Crossref record, with a small difference in title or year; 35 of the 35 references it cites were found in a registry or an index.

Activation and Role of MAP Kinase-Dependent Pathways in Retinal Pigment Epithelium Cells: JNK1, P38 Kinase, and Cell Death

Hecquet, Christiane, Lefevre, Gae¨lle, Valtink, Monika, Engelmann, Katrin, Mascarelli, Frederic·2003·Investigative Opthalmology & Visual Science
DOI 10.1167/iovs.02-0519
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Abstract

PURPOSE: Retinal pigment epithelial (RPE) cell death is an important step in the pathogenesis of ocular diseases. JNK1 and P38 kinase, two stress-activated kinases, play key roles relaying stress signals leading to cell death through cyclin D1 and c-Myc. Recently, stress-activated kinases have been shown to regulate cell proliferation. In the current study, the involvement of the JNK1 and P38 kinase signaling pathways in RPE cell proliferation and death was investigated. METHODS: RPE cell proliferation was stimulated with 10% fetal calf serum (FCS). Activation of the JNK1 and P38 kinase cascades and their potential targets was detected by Western blot analysis. Pharmacologic inhibitors and activators, and antisense oligodeoxynucleotides (ODN) directed against the stress kinases were used to analyze the signaling involved in RPE cell death. RESULTS: P38 and JNK1 and their respective upstream activating kinases, MKK3/6 and -4, were all transiently activated in FCS-stimulated RPE cell cultures. Ras controlled only the activation of JNK1, whereas Rho transmitted the activation of both JNK1 and P38, suggesting parallel signaling pathways and cross talk between the two kinases. Pharmacologic inhibition of JNK1 did not affect cell proliferation in FCS-stimulated cells. Inactivation of P38 kinase and antisense ODN-induced downregulation of P38 kinase also had no affect on cell proliferation. Long-term, high-level activation of JNK1 and P38 kinase occurred during serum depletion-induced RPE cell death. Overactivation of JNK1 and P38 kinase was also observed during pharmacologically induced cell death, suggesting that this process is common to RPE cell-death-signaling pathways induced by various stress stimuli. Cell death mediated by the overactivation of JNK1 and P38 kinase was cyclin D1- and c-Myc-independent. CONCLUSIONS: The inhibition of JNK1 or P38 kinase had no effect on FCS-stimulated proliferation of RPE cells, whereas the overactivation of these two enzymes was involved in RPE cell death in FCS-depleted cultures. Parallel upstream signaling pathways and cross talk between the two kinases suggest that the regulation of signaling in RPE cell death is complex.

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Crossref · 10.1167/iovs.02-0519

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Metadata

Authors
Hecquet, C., Lefevre, G., Valtink, M., Engelmann, K., & Mascarelli, F.
Affiliations
  • Centre National de la Recherche Scientifique (FR)
  • From the Cordeliers Biomedical Institute, National Institute of Health and Medical Research, Unit 450, National Center for Scientific Research, Paris, France; and the
  • University Medical Center Hamburg-Eppendorf (DE)
ORCID
Venue
Investigative Opthalmology & Visual Science
Publisher
Association for Research in Vision and Ophthalmology (ARVO)
Published
2003-03-01
Volume
44
Issue
3
Pages
1320
ISSN
  • 0146-0404 (ISSN-L)
  • 1552-5783
DOI
10.1167/iovs.02-0519
OpenAlex
W2074266196
Cited by
29
References
35
Citations by year
2026: 1 · 2022: 1 · 2018: 2 · 2017: 1 · 2016: 2 · 2014: 2 · 2013: 1
FWCI
3.54
Type
journal article
Language
en
Open access
closed
Locations
  • Investigative Ophthalmology & Visual Science (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Health Sciences › Medicine › Ophthalmology › Retinal Development and Disorders
Keywords
retinal pigment epithelium, JNK1, p38 MAPK, stress-activated kinases, cell death, cell proliferation, serum deprivation, Ras signaling, Rho GTPase signaling, MKK3/6, MKK4, cyclin D1, c-Myc
MeSH terms
Cell Division, Cells, Cultured, Enzyme Activation, Enzyme Inhibitors, Humans, Pigment Epithelium of Eye, Protein-Tyrosine Kinases, Blotting, Western, Down-Regulation, Apoptosis, Calcium-Calmodulin-Dependent Protein Kinases, Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase Kinases, MAP Kinase Signaling System, p38 Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 8, MAP Kinase Kinase 3, MAP Kinase Kinase 6, MAP Kinase Kinase 4

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