ArticleInvestigative ophthalmology & visual science2011
Hyperosmotic stress-induced corneal epithelial cell death through activation of Polo-like kinase 3 and c-Jun.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Expression of tardigrade extremotolerance-associated proteins improves recovery but not acute stress response of human microvascular endothelial cells.Scientific reports · 2026Article
- Current and Developing Therapeutics for Dry Eye Disease: Targeting Ion Channels.Current issues in molecular biology · 2026Review
- A hydrogel platform delivering mesenchymal stem cell lysate for potential myocardial tissue repair.Frontiers in bioengineering and biotechnology · 2026Article
- Trigger Factors in Recurrent Corneal Erosion Syndrome.Journal of clinical medicine · 2025Article
- Cellular osmoregulation enhances porcine embryo development by restoring zygotic genome activation via metabolic-epigenetic crosstalk.Cellular & molecular biology letters · 2025Article
- Upregulations of SNAT2 and GLS-1 Are Key Osmoregulatory Responses of Human Corneal Epithelial Cells to Hyperosmotic Stress.Journal of proteome research · 2025Article
- Review
- Physiological Effects of Soat1 Inactivation on Homeostasis of the Mouse Ocular Surface.Investigative ophthalmology & visual science · 2024Article
- Autophagy is involved in degradation of AQP1 in response to an acute decrement in tonicity.iScience · 2023Article
- Ions, the Movement of Water and the Apoptotic Volume Decrease.Frontiers in cell and developmental biology · 2020Review
- Different Effects of Pro-Inflammatory Factors and Hyperosmotic Stress on Corneal Epithelial Stem/Progenitor Cells and Wound Healing in Mice.Stem cells translational medicine · 2019Article
- Article
- Article
- Rapamycin Prolongs the Survival of Corneal Epithelial Cells in Culture.Scientific reports · 2017Article
- Cytoskeletal architecture and cell motility remain unperturbed in mouse embryonic fibroblasts from Plk3 knockout mice.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- The role of Plk3 in oncogenesis.Oncogene · 2016Review
- Article
- Article
- Osmotic stress-induced phosphorylation of H2AX by polo-like kinase 3 affects cell cycle progression in human corneal epithelial cells.The Journal of biological chemistry · 2014Article
- Nuclear receptor LRH-1/NR5A2 is required and targetable for liver endoplasmic reticulum stress resolution.eLife · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeHyperosmotic stress causes cell shrinkage, perturbs cell function, and damages DNA, resulting in cell cycle arrest and apoptosis. In the present study, the authors explore the mechanism involving hyperosmotic stress-induced activation of c-Jun/AP-1 through a novel Plk3 pathway in human corneal epithelial cells.
methodsHuman primary corneal epithelial cells and cell line were cultured in a serum-free keratinocyte medium and DMEM/F12 medium containing 10% FBS in a 37°C incubator supplied with 5% CO(2), respectively. Western blot analysis was used to determine protein expression and phosphorylation levels. Protein kinase activities were measured by immunocomplex kinase assay. Cell viability and apoptosis were determined by MTT assay and caspase-3 (DEVDase) activity.
resultsIt was found that hyperosmotic stress-induced increases in the phosphorylation of c-Jun, resulting in apoptosis through the activation of Plk3 in human corneal epithelial cells. Plk3 was activated by extracellular hyperosmotic stress to directly phosphorylate c-Jun in the serine 63 and 73 residues. Hyperosmotic stress-induced c-Jun phosphorylation was enhanced by overexpression of constitutively positive Plk3 mutants and suppressed by the knockdown of Plk3 mRNA with Plk3-specific siRNA. Further studies indicated that the phosphorylation of c-Jun by Plk3 was responsible for hyperosmotic stress-induced apoptosis, which was independent from activation of the JNK signaling pathway in human corneal epithelial cells.
conclusionsThese results, for the first time, provide a novel and alternative signaling mechanism that involves hyperosmotic stress-induced activation of the Plk3 pathway in addition to JNK/p38 MAPK pathways to regulate the c-Jun/AP-1 transcriptional complex and human corneal epithelial cell fate.
Indexed as
Identifiers
What OpenQuestion holds
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.