Purpose: The aim of this study was to identify gene expression profiles distinguishing alpha-particle (211)At and (60)Co irradiation.
Materials And Methods: Gene expression microarray profiling was performed using total RNA from confluent human fibroblasts 5 hours after exposure to (211)At labeled trastuzumab monoclonal antibody (0.25, 0.5, and 1 Gy) and (60)Co (1, 2, and 3 Gy).
Results: We report gene expression profiles that distinguish the effect different radiation qualities and absorbed doses have on cellular functions in human fibroblasts. In addition, we identified commonly expressed transcripts between (211)At and (60)Co irradiation. A greater number of transcripts were modulated by (211)At than (60)Co irradiation. In addition, down-regulation was more prevalent than up-regulation following (211)At irradiation. Several biological processes were enriched for both irradiation qualities such as transcription, cell cycle regulation, and cell cycle arrest, whereas mitosis, spindle assembly checkpoint, and apoptotic chromosome condensation were uniquely enriched for alpha particle irradiation.
Conclusions: LET-dependent transcriptional modulations were observed in human fibroblasts 5 hours after irradiation exposure. These findings suggest that in comparison with (60)Co, (211)At has the clearest influence on both tumor protein p53-activated and repressed genes, which impose a greater overall burden to the cell following alpha particle irradiation.
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http://dx.doi.org/10.3109/09553002.2013.746751 | DOI Listing |
iScience
January 2025
Department of Vascular Surgery, Lausanne University Hospital (CHUV), Lausanne, Switzerland.
Aging is accompanied by a decline in neovascularization potential and increased susceptibility to ischemic injury. Here, we confirm the age-related impaired neovascularization following ischemic leg injury and impaired angiogenesis. The age-related deficits in angiogenesis arose primarily from diminished EC proliferation capacity, but not migration or VEGF sensitivity.
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January 2025
Computational Biology Branch, National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, USA.
The regulation of gene expression relies on the coordinated action of transcription factors (TFs) at enhancers, including both activator and repressor TFs. We employed deep learning (DL) to dissect HepG2 enhancers into positive (PAR), negative (NAR), and neutral activity regions. Sharpr-MPRA and STARR-seq highlight the dichotomy impact of NARs and PARs on modulating and catalyzing the activity of enhancers, respectively.
View Article and Find Full Text PDFiScience
January 2025
Mammalian Embryo and Stem Cell Group, University of Cambridge, Department of Physiology, Development and Neuroscience, Downing Street, Cambridge CB2 3DY, UK.
The implantation of the mouse blastocyst initiates a complex sequence of tissue remodeling and cell differentiation events required for morphogenesis, during which the extraembryonic primitive endoderm transitions into the visceral endoderm. Through single-cell RNA sequencing of embryos at embryonic day 5.0, shortly after implantation, we reveal that this transition is driven by dynamic signaling activities, notably the upregulation of BMP signaling and a transient increase in Sox7 expression.
View Article and Find Full Text PDFClin Cosmet Investig Dermatol
January 2025
Department of Dermatology, Candidate Branch of National Clinical Research Centre for Skin and Immune Diseases, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, People's Republic of China.
Dystrophic epidermolysis bullosa (DEB) is a heterogeneous and rare genetic skin disease caused by mutations in the gene, which encodes Type VII collagen. The absence or dysfunction of Type VII collagen can cause the dense lower layer of the basal membrane zone of the skin to separate from the dermis, leading to blister formation and various complications. In different DEB subtypes, the severity of the phenotype is associated, to some extent, with the outcome of Type VII collagen caused by mutations in the gene, which may be reduced in expression, remarkably reduced, or completely absent.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of Rheumatism and Immunity, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, People's Republic of China.
Background: Ankylosing spondylitis (AS) is a chronic autoimmune disease characterized by inflammation of the sacroiliac joints and spine. Cuproptosis is a newly recognized copper-induced cell death mechanism. Our study explored the novel role of cuproptosis-related genes (CRGs) in AS, focusing on immune cell infiltration and molecular clustering.
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