We investigated potential germline-specific radiosensitive biomarkers in the testes of large Japanese field mice (Apodemus speciosus) exposed to low-dose-rate (LDR) radiation after the Fukushima accident. Fukushima wild mice testes were analysed via RNA-sequencing to identify genes differentially expressed in the breeding and non-breeding seasons when compared to controls. Results revealed significant changes during the breeding season, with Lsp1 showing a considerable upregulation, while Ptprk and Tspear exhibited significant reductions. Conversely, in the non-breeding season, Fmo2 and Fmo2 (highly similar) were significantly upregulated in radiation-exposed Fukushima mice. qPCR analysis results were consistent with transcriptome sequencing, detecting Lsp1 and Ptprk regulation in the testes of Fukushima mice. While differences in gene expression were observed, these do not imply any causal association between the identified biomarkers and chronic LDR exposure, as other factors such as the environment and developmental age may contribute. This study provides valuable insights into the reproductive biology is affected by environmental radiation and highlights the value of assessing the effects of chronic LDR radiation exposure on testicular health in wild mice.
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http://dx.doi.org/10.1002/2211-5463.13927 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037.
is one of the three most frequently mutated genes in age-related clonal hematopoiesis (CH), alongside and (. CH can progress to myeloid malignancies including chronic monomyelocytic leukemia (CMML) and is also strongly associated with inflammatory cardiovascular disease and all-cause mortality in humans. DNMT3A and TET2 regulate DNA methylation and demethylation pathways, respectively, and loss-of-function mutations in these genes reduce DNA methylation in heterochromatin, allowing derepression of silenced elements in heterochromatin.
View Article and Find Full Text PDFPLoS One
January 2025
Laboratório de Imunologia Celular (LIM-17), Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Background: NETosis is recognized as an important source of autoantigens. Therefore, we hypothesized whether the pristane-induced lupus mice model shows early activation of neutrophils, the presence of low-density granulocytes (LDGs), and neutrophil extracellular traps (NETs) release, which could contribute to the development of a lupus phenotype.
Methods: Twelve female wild-type Balb/c mice were intraperitoneally injected with pristane (n = 6; pristane group) or saline (n = 6; control group).
PLoS One
January 2025
Ionis Pharmaceuticals, Inc., Carlsbad, CA, United States of America.
Lateral Meningocele Syndrome (LMS), a disorder associated with NOTCH3 pathogenic variants, presents with neurological, craniofacial and skeletal abnormalities. Mouse models of the disease exhibit osteopenia that is ameliorated by the administration of Notch3 antisense oligonucleotides (ASO) targeting either Notch3 or the Notch3 mutation. To determine the consequences of LMS pathogenic variants in human cells and whether they can be targeted by ASOs, induced pluripotent NCRM1 and NCRM5 stem (iPS) cells harboring a NOTCH36692-93insC insertion were created.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Division of Neurogeriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden.
Background: Alzheimer's disease (AD) is associated with synaptic and memory dysfunction. A pathological hallmark of the disease is reactive astrogliosis, with reactive astrocytes surrounding amyloid plaques in the brain. Astrocytes have also been shown to be actively involved in disease progression, nevertheless, mechanistic information about their role in synaptic transmission during AD pathology is lacking.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
Background: Compelling evidence has shown that long non-coding RNAs (lncRNAs) contribute to Alzheimer's disease (AD) pathogenesis including β-amyloid plaque deposition (Aβ) and intracellular neurofibrillary tangles. In this study, we aimed to investigate the critical role of lncRNA Gm20063 in AD.
Method: Six-month-old male APP/PS1 transgenic mice and wild type (WT) C57BL/6 (B6) littermates were obtained from the Nanjing University Animal Model Research Center.
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