Ionizing Radiation (IR), especially at high doses, induces cellular senescence in exposed cultures. IR also induces "bystander effects" through signals released from irradiated cells, and these effects include many of the same outcomes observed following direct exposure. Here, we investigate if radiation can cause senescence through a bystander mechanism. Control cultures were exposed directly to 0, 0.1, 2, and 10 Gy. Unirradiated cells were treated with medium from irradiated cultures or with exosomes extracted from irradiated medium. The level of senescence was determined post-treatment (24 h, 15 days, 30 days, and 45 days) by β-galactosidase staining. Media from cultures exposed to all four doses, and exosomes from these cultures, induced significant senescence in recipient cultures. Senescence levels were initially low at the earliest timepoint, and peaked at 15 days, and then decreased with further passaging. These results demonstrate that senescence is inducible through a bystander mechanism. As with other bystander effects, bystander senescence was induced by a low radiation dose. However, unlike other bystander effects, cultures recovered from bystander senescence after repeated passaging. Bystander senescence may be a potentially significant effect of exposure to IR, and may have both beneficial and harmful effects in the context of radiotherapy.
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http://dx.doi.org/10.3390/biology9080191 | DOI Listing |
Alzheimers Dement
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University of Texas Medical Branch, Galveston, TX, USA.
Background: Aging, tau pathology, and chronic inflammation in the brain play crucial roles in neuroinflammation, synaptic loss, neurodegeneration, and cognitive decline in tauopathies, such as Alzheimer's disease. However, the molecular mechanisms that trigger aberrant chronic inflammatory signaling in tauopathies are poorly understood.
Method: We utilized brain tissues from tauopathy patients and the tauopathy mouse models.
Curr Opin Rheumatol
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Centre for Arthritis and Musculoskeletal Health, University of Aberdeen, Aberdeen, UK.
Purpose Of Review: Giant cell arteritis (GCA) is an age-related autoimmune disease with a complex pathogenesis that involves several pathogenic mechanisms. This review provides recent critical insights into novel aspects of GCA pathogenesis.
Recent Findings: The use of novel approaches, including multiomic techniques, has uncovered notable findings that broaden the understanding of GCA pathogenesis.
Eur Heart J
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Medicine and Medicine Sub-Specialties Department, Cardio Renal Program, UOC Nephrology, Dialysis and Adult Renal Transplant Program, IRCCS Ca' Granda Foundation, Ospedale Maggiore Policlinico, Milan, Italy.
Front Immunol
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Núcleo de Doenças Infecciosas, Universidade Federal do Espírito Santo, Vitória, Brazil.
Cytotoxic activity is a hallmark of the immunopathogenesis in human cutaneous leishmaniasis (CL). In this study, we identified accumulation of CD4 granzyme B producing T cells with increased cytotoxic capacity in CL lesions. These cells showed enhanced expression of activating NK receptors (NKG2D and NKG2C), diminished expression of inhibitory NKG2A, along with the upregulation of the senescence marker CD57.
View Article and Find Full Text PDFCell Commun Signal
October 2024
Department of Effects and Risks of Ionizing & Non-Ionizing Radiation, Federal Office for Radiation Protection (BfS), Neuherberg, Germany.
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