ArticleThe Journal of biological chemistry2014
Osmotic stress-induced phosphorylation of H2AX by polo-like kinase 3 affects cell cycle progression in human corneal epithelial cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Trigger Factors in Recurrent Corneal Erosion Syndrome.Journal of clinical medicine · 2025Article
- Inhibition of PLK3 Attenuates Tubular Epithelial Cell Apoptosis after Renal Ischemia-Reperfusion Injury by Blocking the ATM/P53-Mediated DNA Damage Response.Oxidative medicine and cellular longevity · 2022Article
- The Role of Nuclear Factor of Activated T Cells 5 in Hyperosmotic Stress-Exposed Human Lens Epithelial Cells.International journal of molecular sciences · 2021Article
- Hyperosmotic stress:Nucleus (Austin, Tex.) · 2020Article
- γH2AX in the S Phase after UV Irradiation Corresponds to DNA Replication and Does Not Report on the Extent of DNA Damage.Molecular and cellular biology · 2020Article
- hADSCs derived extracellular vesicles inhibit NLRP3inflammasome activation and dry eye.Scientific reports · 2020Article
- Article
- Histone acetyltransferase and Polo-like kinase 3 inhibitors prevent rat galactose-induced cataract.Scientific reports · 2019Article
- Hypoosmotic stress induces R loop formation in nucleoli and ATR/ATM-dependent silencing of nucleolar transcription.Nucleic acids research · 2019Article
- 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
- Response of Mouse Zygotes Treated with Mild Hydrogen Peroxide as a Model to Reveal Novel Mechanisms of Oxidative Stress-Induced Injury in Early Embryos.Oxidative medicine and cellular longevity · 2016Article
- Effects of hyperthermia on DNA repair pathways: one treatment to inhibit them all.Radiation oncology (London, England) · 2015Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Increased concentrations of extracellular solutes affect cell function and fate by stimulating cellular responses, such as evoking MAPK cascades, altering cell cycle progression, and causing apoptosis. Our study results here demonstrate that hyperosmotic stress induced H2AX phosphorylation (γH2AX) by an unrevealed kinase cascade involving polo-like kinase 3 (Plk3) in human corneal epithelial (HCE) cells. We found that hyperosmotic stress induced DNA-double strand breaks and increased γH2AX in HCE cells. Phosphorylation of H2AX at serine 139 was catalyzed by hyperosmotic stress-induced activation of Plk3. Plk3 directly interacted with H2AX and was colocalized with γH2AX in the nuclei of hyperosmotic stress-induced cells. Suppression of Plk3 activity by overexpression of a kinase-silencing mutant or by knocking down Plk3 mRNA effectively reduced γH2AX in hyperosmotic stress-induced cells. This was consistent with results that show γH2AX was markedly suppressed in the Plk3(-/-) knock-out mouse corneal epithelial layer in response to hyperosmotic stimulation. The effect of hyperosmotic stress-activated Plk3 and increased γH2AX in cell cycle progression showed an accumulation of G2/M phase, altered population in G1 and S phases, and increased apoptosis. Our results for the first time reveal that hyperosmotic stress-activated Plk3 elicited γH2AX. This Plk3-mediated activation of γH2AX subsequently regulates the cell cycle progression and cell fate.
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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.