microRNA-7 Protects Against 1-Methyl-4-Phenylpyridinium Iodide-Induced Cell Apoptosis in SH-SY5Y Cells by Directly Targeting Krüpple-Like Factor 4.

This study intended to investigate the role and underling mechanism of microRNA-7 (miR-7) on neuronal death in Parkinson's disease (PD). Human neuroblastoma cell line SH-SY5Y was employed and 1-methyl-4-phenylpyridinium iodide [MPP(+)] was used to generate PD model in vitro. Furthermore, an upregulation of miR-7 was performed in SH-SY5Y by transfection with miR-7 mimics. Cell viability and cell apoptosis were determined. Moreover, the target and the mechanism of miR-7 in MPP(+)-induced cell death were also investigated. The upregulation of miR-7 promoted cell viability and suppressed cell apoptosis in MPP(+)-treated SH-SY5Y cells. Furthermore, miR-7 could directly bind to the 3'-untranslated region of Krüppel-like factor 4 (KLF4, positions 574-580). Moreover, knockdown of KLF4 by the specific siRNA inhibited SH-SY5Y apoptosis under MPP(+) treatment. In addition, KLF4 overexpression apparently attenuated the protective effect of miR-7 in MPP(+)-induced SH-SY5Y apoptosis. This study indicated that miR-7 protects from MPP(+)-induced cell apoptosis in SH-SY5Y by directly targeting KLF4.

Analyzing time-series microarray data reveals key genes in spinal cord injury.

Although many scholars have utilized high-throughput microarrays to delineate gene expression patterns after spinal cord injury (SCI), no study has evaluated gene changes in raphe magnus (RM) and somatomotor cortex (SMTC), two areas in brain primarily affected by SCI. In present study, we aimed to analyze the differentially expressed genes (DEGs) of RM and SMTC between SCI model and sham injured control at 4, 24 h, 7, 14, 28 days, and 3 months using microarray dataset GSE2270 downloaded from gene expression omnibus and unpaired significance analysis of microarray method. Protein-protein interaction (PPI) network was constructed for DEGs at crucial time points and significant biological functions were enriched using DAVID. The results indicated that more DEGs were identified at 14 days in RM and at 4 h/3 months in SMTC after SCI. In the PPI network for DEGs at 14 days in RM, interleukin 6, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), FBJ murine osteosarcoma viral oncogene homolog (FOS), tumor necrosis factor, and nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor) were the top 5 hub genes; In the PPI network for DEGs at 3 months in SMTC, the top 5 hub genes were ubiquitin B, Ras-related C3 botulinum toxin substrate 1 (rho family, small GTP binding protein Rac1), FOS, Janus kinase 2 and vascular endothelial growth factor A. Hedgehog and Wnt signaling pathways were the top 2 significant pathways in RM. These hub DEGs and pathways may be underlying therapeutic targets for SCI.

Epileptiform Discharges and Frontal Paroxysmal EEG Abnormality Act as Predictive Marker for Subsequent Epilepsy in Children With Complex Febrile Seizures.

Using electroencephalography (EEG) for diagnosing subsequent epilepsy in children after febrile seizure (FS) is not common. The present study investigates the relationship between epileptiform discharges and subsequent epilepsy, and looks for the predictive marker for this disorder. A total of 378 children with complex FS and whose EEG showed epileptiform discharges or normal EEG were included. Development of FS was compared between those with epileptiform discharges and those with normal EEG. Risk factors were analyzed using multivariate logistic regression to clarify their effects on subsequent epilepsy. The association between generalized or focal EEG localization, and between frontal epileptiform discharges and subsequent epilepsy, were analyzed. Among 378 patients with complex FS, 51 showed epileptiform discharges. History of epilepsy, frontal seizure, number of FS, and prolonged seizure were the risk factors for epileptiform discharge. Subsequent epilepsy was significantly frequent in patients with more than 2 risk factors (odds ratio [OR] = 17; 95% confidence interval [CI] = 4.1-29.6). Prolonged seizure (OR = 4.98; 95% CI = 1.63-13.29), FS number (OR = 2.96; 95% CI = 1.23-10.51), and family history of epilepsy (OR = 2.67; 95% CI = 1.05-7.63) were significantly correlated with subsequent epilepsy. Of 9 patients with paroxysms in the frontal region, 8 (88.9%) developed epilepsy. There was concordance between frontal epileptiform discharges and subsequent epilepsy (κ = .901). In conclusion, epileptiform discharges are risk factors for subsequent epilepsy. Frontal paroxysmal EEG is a marker for subsequent epilepsy.