دورية أكاديمية
أعرض في EDS

Effect of the p38 Mitogen-Activated Protein Kinase Signaling Cascade on Radiation Biodosimetry.

التفاصيل البيبلوغرافية
العنوان: Effect of the p38 Mitogen-Activated Protein Kinase Signaling Cascade on Radiation Biodosimetry.
المؤلفون: Broustas CG; Center for Radiological Research, Columbia University Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York., Mukherjee S; Center for Radiological Research, Columbia University Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York., Pannkuk EL; Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC.; Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC., Laiakis EC; Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC.; Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC., Fornace AJ; Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC.; Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC., Amundson SA; Center for Radiological Research, Columbia University Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.
المصدر: Radiation research [Radiat Res] 2022 Jul 01; Vol. 198 (1), pp. 18-27.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Radiation Research Society Country of Publication: United States NLM ID: 0401245 Publication Model: Print Cited Medium: Internet ISSN: 1938-5404 (Electronic) Linking ISSN: 00337587 NLM ISO Abbreviation: Radiat Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Bozeman, MT : Radiation Research Society
Original Publication: Charlottesville, VA : Kluge Carden Jennnings Pub. Co.
مواضيع طبية MeSH: Signal Transduction*/physiology , p38 Mitogen-Activated Protein Kinases*/metabolism, Animals ; Enzyme Activation ; MAP Kinase Signaling System ; Male ; Mammals/metabolism ; Mice ; Mitogen-Activated Protein Kinase Kinases
مستخلص: Radiation biodosimetry based on transcriptomic analysis of peripheral blood is a valuable tool to detect radiation exposure after a radiological/nuclear event and obtain useful biological information that could predict tissue and organismal injury. However, confounding factors, including chronic inflammation or immune suppression, can potentially obscure the predictive power of the method. Members of the p38 mitogen-activated protein kinase (MAPK) family respond to pro-inflammatory signals and environmental stresses, whereas genetic ablation of the p38 signaling pathway in mice leads to reduced susceptibility to collagen-induced arthritis and experimental autoimmune encephalomyelitis that model human rheumatoid arthritis and multiple sclerosis, respectively. p38 is normally regulated by the MAP3K-MAP2K pathway in mammalian cells. However, in T cells there is an alternative pathway for p38 activation that plays an important role in antigen-receptor-activated T cells and participates in immune and inflammatory responses. To examine the role of p38 in response to radiation, we used two mouse models expressing either a p38α dominant negative (DN) mutation that globally suppresses p38 signaling or a p38αβ double-knock-in (DKI) mutant, which inhibits specifically T-cell receptor activation. We exposed p38 wild-type (p38WT) and mutant male mice to 7 Gy X rays and 24 h later whole blood was isolated subjected to whole-genome microarray and gene ontology analysis. Irradiation of p38WT mice led to a significant overrepresentation of pathways associated with morbidity and mortality, as well as organismal cell death. In contrast, these pathways were significantly underrepresented in p38DN and p38DKI mutant mice, suggesting that p38 attenuation may protect blood cells from the deleterious effects of radiation. Furthermore, radiation exposure in p38 mutant mice resulted in an enrichment of phagocytosis-related pathways, suggesting a role for p38 signaling in restricting phagocytosis of apoptotic cells after irradiation. Finally, despite the significant changes in gene expression, it was still feasible to identify a panel of genes that could accurately distinguish between irradiated and control mice, irrespective of p38 status.
(©2022 by Radiation Research Society. All rights of reproduction in any form reserved.)
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معلومات مُعتمدة: U19 AI067773 United States AI NIAID NIH HHS
المشرفين على المادة: EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
تواريخ الأحداث: Date Created: 20220330 Date Completed: 20220712 Latest Revision: 20230703
رمز التحديث: 20240829
مُعرف محوري في PubMed: PMC9310339
DOI: 10.1667/RADE-21-00240.1
PMID: 35353886
قاعدة البيانات: MEDLINE
الوصف
تدمد:1938-5404
DOI:10.1667/RADE-21-00240.1