Tweedie David, Rachmany Lital, Kim Dong Seok, Rubovitch Vardit, Lehrmann Elin, Zhang Yongqing, Becker Kevin G, Perez Evelyn, Pick Chaim G, Greig Nigel H
Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Department of Anatomy and Anthropology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv 69978, Israel.
J Neurosci Methods. 2016 Oct 15;272:4-18. doi: 10.1016/j.jneumeth.2016.02.003. Epub 2016 Feb 8.
Neurological dysfunction after traumatic brain injury (TBI) poses short-term or long-lasting health issues for family members and health care providers. Presently there are no approved medicines to treat TBI. Epidemiological evidence suggests that TBI may cause neurodegenerative disease later in life. In an effort to illuminate target cellular processes for drug development, we examined the effects of a mild TBI on hippocampal gene expression in mouse.
mTBI was induced in a closed head, weight drop-system in mice (ICR). Animals were anesthetized and subjected to mTBI (30g). Fourteen days after injury the ipsilateral hippocampus was utilized for cDNA gene array studies. mTBI animals were compared with sham-operated animals. Genes regulated by TBI were identified to define TBI-induced physiological/pathological processes. mTBI regulated genes were divided into functional groupings to provide gene ontologies. Genes were further divided to identify molecular/cellular pathways regulated by mTBI.
Numerous genes were regulated after a single mTBI event that mapped to many ontologies and molecular pathways related to inflammation and neurological physiology/pathology, including neurodegenerative disease.
These data illustrate diverse transcriptional changes in hippocampal tissues triggered by a single mild injury. The systematic analysis of individual genes that lead to the identification of functional categories, such as gene ontologies and then molecular pathways, illustrate target processes of relevance to TBI pathology. These processes may be further dissected to identify key factors that can be evaluated at the protein level to highlight possible treatments for TBI in human disease and potential biomarkers of neurodegenerative processes.
创伤性脑损伤(TBI)后的神经功能障碍给家庭成员和医护人员带来了短期或长期的健康问题。目前尚无获批用于治疗TBI的药物。流行病学证据表明,TBI可能在日后引发神经退行性疾病。为了阐明药物研发的目标细胞过程,我们研究了轻度TBI对小鼠海马体基因表达的影响。
在小鼠(ICR)的闭合性头部重量坠落系统中诱导轻度创伤性脑损伤(mTBI)。动物麻醉后接受mTBI(30g)。损伤后14天,取同侧海马体用于cDNA基因芯片研究。将mTBI动物与假手术动物进行比较。鉴定出受TBI调控的基因,以确定TBI诱导的生理/病理过程。将mTBI调控的基因分为功能组以提供基因本体论。进一步划分基因以鉴定受mTBI调控的分子/细胞途径。
单次mTBI事件后,许多基因受到调控,这些基因映射到许多与炎症以及神经生理/病理(包括神经退行性疾病)相关的本体论和分子途径。
这些数据表明,单次轻度损伤会引发海马组织中多种转录变化。对单个基因进行系统分析,从而确定功能类别,如基因本体论,然后是分子途径,这阐明了与TBI病理学相关的目标过程。这些过程可能会被进一步剖析,以识别可在蛋白质水平进行评估的关键因素,从而突出针对人类疾病中TBI的可能治疗方法以及神经退行性过程的潜在生物标志物。