AIM. Previous studies have provided insights into complex immune system changes caused by ischemic stroke (IS), while detailed reports are lacking especially in peripheral blood. Here, we sought to identify genetic biomarkers in immune system which significantly associated with the occurrence of IS and explore candidate drugs that can regulate the process. We also investigated whether gene expression alternation of immune genes contributed to differential distribution of immune cells in peripheral blood following IS. Method. 108 IS samples and 47 matched controls were obtained from the GEO database. Immune-related genes (IRGs) and their associated drugs were collected from the ImmPort and PharmGBK databases, respectively. Random forest (RF) regression and least absolute shrinkage and selection operator (LASSO) logistic regression were applied to identify immune-related genetic biomarkers (IRGBs) of IS, and accuracy was verified using neural network models. Finally, proportion changes of various immune cells in peripheral blood of IS patients were evaluated using CIBERSORT and xCell and correlation analyses were performed between IRGBs and differentially distributed immune cells. Results. A total of 537 genes were differentially expressed between IS and control samples. Four immune-related differential expressed genes identified by regression analysis presented strong predictive power ( AUC = 0.909 ) which we suggeseted them as immune-related genetic biomarkers (IRGBs). We also demonstrated six immune-related genes targeted by known drugs. In addition, post-IS immune system presented an increase in the proportion of innate immune cells and a decrease in adaptive immune cells in the peripheral circulation, and IRGBs showing significance were associated with this process.Conclusion. The study identified CARD11, ICAM2, VIM, and CD19 as immune-related genetic biomarkers of IS. Six immune-related DEGs targeted by known drugs were found and provide new candidate drug targets for modulating the post-IS immune system. The innate immune cells and adaptive immune cells are diversified in the post-IS immune system, and IRGBs might play important role during this process.
The COVID-19 pandemic has caused millions of deaths and remains a major public health burden worldwide. Previous studies found that a large number of COVID-19 patients and survivors developed neurological symptoms and might be at high risk of neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). We aimed to explore the shared pathways between COVID-19, AD, and PD by using bioinformatic analysis to reveal potential mechanisms, which may explain the neurological symptoms and degeneration of brain that occur in COVID-19 patients, and to provide early intervention. In this study, gene expression datasets of the frontal cortex were employed to detect common differentially expressed genes (DEGs) of COVID-19, AD, and PD. A total of 52 common DEGs were then examined using functional annotation, protein–protein interaction (PPI) construction, candidate drug identification, and regulatory network analysis. We found that the involvement of the synaptic vesicle cycle and down-regulation of synapses were shared by these three diseases, suggesting that synaptic dysfunction might contribute to the onset and progress of neurodegenerative diseases caused by COVID-19. Five hub genes and one key module were obtained from the PPI network. Moreover, 5 drugs and 42 transcription factors (TFs) were also identified on the datasets. In conclusion, the results of our study provide new insights and directions for follow-up studies of the relationship between COVID-19 and neurodegenerative diseases. The hub genes and potential drugs we identified may provide promising treatment strategies to prevent COVID-19 patients from developing these disorders.
The reversal of loss of the critical size of skeletal muscle is urgently required using biomaterial scaffolds to guide tissue regeneration. In this work, coaxial electrospun magnetic nanofibrous scaffolds were fabricated, with gelatin (Gel) as the shell of the fiber and polyurethane (PU) as the core. Iron oxide nanoparticles (Mag) of 10 nm diameter were added to the shell and core layer. Myoblast cells (C2C12) were cultured on the magnetic scaffolds and exposed to the applied magnetic fields. A mouse model of skeletal muscle injury was used to evaluate the repair guided by the scaffolds under the magnetic fields. It was shown that VEGF secretion and MyoG expression for the myoblast cells grown on the magnetic scaffolds under the magnetic fields were significantly increased, while, the gene expression of Myh4 was up-regulated. Results from an in vivo study indicated that the process of skeletal muscle regeneration in the mouse muscle injury model was accelerated by using the magnetic actuated strategy, which was verified by histochemical analysis, immunofluorescence staining of CD31, electrophysiological measurement and ultrasound imaging. In conclusion, the integration of a magnetic scaffold combined with the extra magnetic fields enhanced myoblast differentiation and VEGF secretion and accelerated the defect repair of skeletal muscle in situ.
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