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Nucleo-cytoplasmic RNA distribution responsible for maintaining neuroinflammatory microenvironment.

ABSTRACT: Characteristics of subcellular localization of RNAs are closely associated with their transcriptional outputs and, therefore, involved in the physiological process of many cases of central nervous system diseases, such as hemorrhagic stroke, which threatens millions of people and causes of death and long-term disability world-wide. Using whole-transcriptome sequencing (RNA-seq), here we report a subcellular gene profiling during hemorrhagic damage. Differentially expressed genes owing to spatial distribution of oxyhemoglobin (oxy-hb) treated-microglial nuclear and cytoplasmic fractions were enriched in biological processes in RNA metabolism and RNA splicing regardless of the duration of stimulation; while hemorrhage-induced differentially expressed genes played roles in inflammation regardless of the duration of stimulation. Interestingly, nuclear-retained intron of microglial nucleocytoplasmic transport genes may result in their down-regulation in 24 hours of oxy-Hb stimulation. This transcriptome study advances our understanding of the contributor of subcellular components, revealing new insights into cytoplasmic non-coding RNAs in response to hemorrhage and provide a resource for investigating comparable diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE160934 | GEO | 2021/02/26

REPOSITORIES: GEO

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Project description:The etiology of trauma-hemorrhage shock-induced acute lung injury has been difficult to elucidate due, at least in part, to the inability of in vivo studies to separate the non-injurious pulmonary effects of trauma-hemorrhage from the tissue injurious ones. To circumvent this in vivo limitation, we utilized a model of trauma-hemorrhagic shock (T/HS) in which T/HS-lung injury was abrogated by dividing the mesenteric lymph duct. In this way, it was possible to separate the pulmonary injurious response from the non-injurious systemic response to T/HS by comparing the pulmonary molecular response of rats subjected to T/HS which did and did not develop lung injury as well as to non-shocked rats. Utilizing high-density oligonucleotide arrays and treatment group comparisons of whole lung tissue collected at 3 hours after the end of the shock or sham-shock period, 139 of the 8,799 assessed genes were differentially expressed. Experiment Overall Design: Four groups of rats (n=3) were studied in order to identify changes in pulmonary gene expression associated with T/HS, both in the presence and absence of lung injury. These included trauma-sham shock (T/SS) rats which had a laparotomy (trauma) but were not subjected to hemorrhagic shock. These rats had no lung injury and served as controls for rats which were subjected to T/HS (laparotomy plus 90 min of shock) and had lung injury. Differences in gene expression between these two groups would represent both the effects of hemorrhagic shock as well as lung injury. To distinguish the gene response of hemorrhagic shock from the gene response associated with lung injury, gene expression was also compared between T/HS rats (hemorrhage and lung injury) and rats subjected to T/HS plus lymph duct ligation (T/HS-LDL), since the T/HS-LDL rats experienced hemorrhagic shock but had no measurable lung injury. Lastly, to identify hemorrhagic shock- modified genes, the pulmonary gene response of T/HS-LDL (hemorrhage without lung injury) were compared to rats subjected to T/SS plus LDL (no hemorrhage or lung injury). Three hours after the end of the 90 min shock or sham-shock period (i.e. 4.5 hrs after the induction of T/HS), the rats were sacrificed and specimens harvested for genechip analysis and histology.

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Nucleo-cytoplasmic RNA distribution responsible for maintaining neuroinflammatory microenvironment.

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