ArticlePloS one2014
Role of the ERK pathway for oxidant-induced parthanatos in human lymphocytes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Review on Photodynamic Therapy Combined with T-Cell Immunotherapy for Recurrent or Metastatic Nasopharyngeal Carcinoma: Mechanisms, Challenges, and Future Directions.Current treatment options in oncology · 2026Review
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- Thioredoxin Reductase 1 inhibition triggers ferroptosis in KRAS-independent lung cancers.bioRxiv : the preprint server for biology · 2025Article
- Melittin inhibits MPPThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- NOX Family: Regulators of Reactive Oxygen Species Balance in Tumor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Deregulation of New Cell Death Mechanisms in Leukemia.Cancers · 2024Review
- Article
- CASK Mediates Oxidative Stress-Induced Microglial Apoptosis-Inducing Factor-Independent Parthanatos Cell Death via Promoting PARP-1 Hyperactivation and Mitochondrial Dysfunction.Antioxidants (Basel, Switzerland) · 2024Article
- A programmed cell death-related model based on machine learning for predicting prognosis and immunotherapy responses in patients with lung adenocarcinoma.Frontiers in immunology · 2023Article
- Role of Phosphoinositide 3-Kinase in Regulation of NOX-Derived Reactive Oxygen Species in Cancer.Antioxidants (Basel, Switzerland) · 2022Review
- Non-Canonical Programmed Cell Death in Colon Cancer.Cancers · 2022Review
- Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases.International journal of molecular sciences · 2022Review
- Erlotinib protests against LPS-induced parthanatos through inhibiting macrophage surface TLR4 expression.Cell death discovery · 2021Article
- Dexmedetomidine suppresses bupivacaine-induced parthanatos in human SH-SY5Y cells via the miR-7-5p/PARP1 axis-mediated ROS.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy.Journal of Cancer · 2021Review
- Review
- NOX2-Derived Reactive Oxygen Species in Cancer.Oxidative medicine and cellular longevity · 2020Review
- Propofol inhibits parthanatos via ROS-ER-calcium-mitochondria signal pathway in vivo and vitro.Cell death & disease · 2018Article
- Multiple molecular mechanisms form a positive feedback loop driving amyloid β42 peptide-induced neurotoxicity via activation of the TRPM2 channel in hippocampal neurons.Cell death & disease · 2018Article
- Endoplasmic reticulum stress regulates oxygen-glucose deprivation-induced parthanatos in human SH-SY5Y cells via improvement of intracellular ROS.CNS neuroscience & therapeutics · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) are formed by myeloid cells as a defense strategy against microorganisms. ROS however also trigger poly(ADP-ribose) polymerase 1- (PARP-1) dependent cell death (parthanatos) in adjacent lymphocytes, which has been forwarded as a mechanism of immune escape in several forms of cancer. The present study assessed the role of mitogen-activated protein kinases (MAPKs), in particular the extracellular signal-regulated kinase (ERK), in ROS-induced signal transduction leading to lymphocyte parthanatos. We report that inhibitors of ERK1/2 phosphorylation upheld natural killer (NK) cell-mediated cytotoxicity under conditions of oxidative stress and rescued NK cells and CD8(+) T lymphocytes from cell death induced by ROS-producing monocytes. ERK1/2 phosphorylation inhibition also protected lymphocytes from cell death induced by exogenous hydrogen peroxide (H2O2) and from ROS generated by xanthine oxidase or glucose oxidase. Phosphorylation of ERK1/2 was observed in lymphocytes shortly after exposure to ROS. ROS-generating myeloid cells and exogenous H2O2 triggered PARP 1-dependent accumulation of poly ADP-ribose (PAR), which was prevented by ERK pathway inhibitors. ERK1/2 phosphorylation was induced by ROS independently of PARP-1. Our findings are suggestive of a role for ERK1/2 in ROS-induced lymphocyte parthanatos, and that the ERK axis may provide a therapeutic target for the protection of lymphocytes against oxidative stress.
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