Publications by authors named "Bao-Dong He"
Traumatic brain injury (TBI) is an acquired insult to the brain caused by an external mechanical force, potentially resulting in temporary or permanent impairment. Microglia, the resident immune cells of the central nervous system, are activated in response to TBI, participating in tissue repair process. However, the underlying epigenetic mechanisms in microglia during TBI remain poorly understood.
View Article and Find Full Text PDFTraumatic brain injury usually triggers glial scar formation, neuroinflammation, and neurodegeneration. However, the molecular mechanisms underlying these pathological features are largely unknown. Using a mouse model of hippocampal stab injury (HSI), we observed that miR-331, a brain-enriched microRNA, was significantly downregulated in the early stage (0-7 days) of HSI.
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- Traumatic brain injury (TBI) leads to neuronal loss and cognitive issues, prompting interest in promoting neurogenesis as a potential treatment.
- Transglutaminase 2 (TGM2) is found to be crucial for neurogenic processes, showing significant dysregulation post-TBI and possibly serving as a target for advancing neural regeneration.
- Research using a conditional knockout mouse model demonstrated that TGM2 influences neural stem/progenitor cell proliferation, differentiation, and migration, making it a promising therapeutic target for enhancing neurogenesis in the hippocampus after TBI.
A Mouse Model of Neurodegeneration Induced by Blade Penetrating Stab Wound to the Hippocampus.
Biology (Basel)
September 2022
Traumatic brain injury (TBI) is closely associated with the later development of neurodegenerative and psychiatric diseases which are still incurable. Although various animal TBI models have been generated, they usually have weaknesses in standardization, survivability and/or reproducibility. In the present study, we investigated whether applying a blade penetrating stab wound to the hippocampus would create an animal model of cognitive deficits.
View Article and Find Full Text PDFThe embryonic ectoderm development (EED) is a core component of the polycomb-repressive complex 2 (PRC2) whose mutations are linked to neurodevelopmental abnormalities, intellectual disability, and neurodegeneration. Although EED has been extensively studied in neural stem cells and oligodendrocytes, its role in microglia is incompletely understood. Here, we show that microglial EED is essential for synaptic pruning during the postnatal stage of brain development.
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- * This study investigates the role of microglia (a type of brain cell) in response to cortical injury by analyzing gene expression over time and comparing between sexes.
- * Findings indicate that microglia show different gene activity patterns based on time post-injury and sex, suggesting potential pathways for developing targeted treatments for neurodegenerative diseases.