[Research progress of brain-derived microparticles on microglia polarization in radiation-induced brain injury of head and neck tumors].

Radiation brain injury（RBI） is one of the complications of radiotherapy for head and neck malignant tumors, which has a serious impact on the prognosis and quality of life of patients. The existence of radiation-induced brain injury not only limits the radiation therapy dose of head and neck malignant tumors, but also restricts the efficacy of tumor patients, and has a serious impact on the prognosis and quality of life of patients. The pathogenesis of radiation-induced brain injury is not yet completely clear, we use various clinical treatment for radiation brain injury patients to alleviate some clinical symptoms, but it cannot effectively reverse the brain injury process. In recent years, with the further exploration of radiation-induced brain injury and the accumulation of clinical experience, studies have found that microglial polarization plays an important role in radiation-induced brain injury, and brain-derived particles can activate microglia. This article reviews the research progress of brain-derived microparticles on the polarization of microglia in radiation-induced brain injury of head and neck tumors.

Dietary and genetic effects on age-related loss of gene silencing reveal epigenetic plasticity of chromatin repression during aging.

During aging, changes in chromatin state that alter gene transcription have been postulated to result in expression of genes that are normally silenced, leading to deleterious age-related effects on cellular physiology. Despite the prevalence of this hypothesis, it is primarily in yeast that loss of gene silencing with age has been well documented. We use a novel position effect variegation (PEV) reporter in Drosophila melanogaster to show that age-related loss of repressive heterochromatin is associated with loss of gene silencing in metazoans and is affected by Sir2, as it is in yeast. The life span-extending intervention, calorie restriction (CR), delays the age-related loss of gene silencing, indicating that loss of gene silencing is a component of normal aging. Diet switch experiments show that such flies undergo a rapid change in their level of gene silencing, demonstrating the epigenetic plasticity of chromatin during aging and highlighting the potential role of diet and metabolism in chromatin maintenance, Thus, diet and related interventions may be of therapeutic importance for age-related diseases, such as cancer.

RNA editing regulates transposon-mediated heterochromatic gene silencing.

Heterochromatin formation drives epigenetic mechanisms associated with silenced gene expression. Repressive heterochromatin is established through the RNA interference pathway, triggered by double-stranded RNAs (dsRNAs) that can be modified via RNA editing. However, the biological consequences of such modifications remain enigmatic. Here we show that RNA editing regulates heterochromatic gene silencing in Drosophila. We utilize the binding activity of an RNA-editing enzyme to visualize the in vivo production of a long dsRNA trigger mediated by Hoppel transposable elements. Using homologous recombination, we delete this trigger, dramatically altering heterochromatic gene silencing and chromatin architecture. Furthermore, we show that the trigger RNA is edited and that dADAR serves as a key regulator of chromatin state. Additionally, dADAR auto-editing generates a natural suppressor of gene silencing. Lastly, systemic differences in RNA editing activity generates interindividual variation in silencing state within a population. Our data reveal a global role for RNA editing in regulating gene expression.