Ischemic stroke is one of the most common diseases that has a high rate of mortality, and has become a burden to the healthcare system. Previous research has shown that EPH receptor B4 (EphB4) promotes neural stem cell proliferation and differentiation in vitro. However, little is known regarding its role in the neurogenesis of ischemic stroke in vivo. Thus, the present study aimed to verify whether EphB4 was a key regulator of neurogenesis in ischemic stroke in vivo. Cerebral ischemia was induced in C57BL/6J mice via middle cerebral artery occlusion (MCAO), followed by reperfusion. Immunofluorescence staining was performed to evaluate the effect of EphB4 on the neurogenesis in cerebral cortex. The levels of inflammatory cytokines were determined using an ELISA kit. The expression levels of ABL proto‑oncogene 1, non‑receptor tyrosine kinase (ABL1)/Cyclin D1 signaling pathway‑related proteins were detected via western blotting. The current findings indicated that EphB4 expression was significantly increased in the cerebral cortex of MCAO model mice in comparison with sham‑operated mice. Moreover, EphB4 appeared to be expressed in neural stem cells (Nestin+), and persisted as these cells became neuronal progenitors (Sox2+), neuroblasts [doublecortin (DCX)+], and eventually mature neurons [neuronal nuclei (NeuN)+]. Overexpression of EphB4 elevated the number of proliferating (bromodeoxyuridine+, Ki67+) and differentiated cells (Nestin+, Sox2+, DCX+ and NeuN+), indicating the promoting effect of EphB4 on the neurogenesis of ischemic stroke. Furthermore, EphB4 overexpression alleviated the inflammation injury in MCAO model mice. The expression levels of proteins‑related to the ABL1/Cyclin D1 signaling pathway were significantly increased by the overexpression of EphB4, which suggested that restoration of EphB4 promoted the activation of the ABL1/Cyclin D1 signaling pathway. In conclusion, this study contributes to the current understanding of the mechanisms of EphB4 in exerting neurorestorative effects and may recommend a potential new strategy for ischemic stroke treatment.
We report rapid and sensitive phenotyping of bacterial response to antibiotic treatment at single-cell resolution by a Raman-integrated optical mid-infrared photothermal (MIP) microscope. The MIP microscope successfully detected biochemical changes of bacteria in specific to the acting mechanism of erythromycin with 1 h incubation. Compared to Raman spectroscopy, MIP spectroscopy showed a much larger signal-to-noise ratio at the fingerprint region at an acquisition speed as fast as 1 s per spectrum. The high sensitivity of MIP enabled detection of metabolic changes at antibiotic concentrations below minimum inhibitory concentration (MIC). Meanwhile, the single-cell resolution of the technique allowed observation of heteroresistance within one bacterial population, which is of great clinical relevance. This study showcases characterizing antibiotic response as one of the many possibilities of applying MIP microscopy to single-cell biology.
Abstract Background: This study was aimed to investigate the regulatory role of microRNA-210 (miRNA-210) on the progression of liver cancer and Hepatitis B virus (HBV)-associated liver cancer. Methods: The expression of miRNA-210 was detected in liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells by qRT-PCR. MiRNA-210 was silenced in HepG2 and HepG2.2.15 cells by the transfection of miRNA-210 inhibitor. The cell viability and apoptosis was detected by MTT assay and Annexin V-fluorescein isothiocyanate/propidium iodide staining, respectively. The protein expression of EGR3 was detected by Western blot. The regulatory relationship between EGR3 and miRNA-210 was predicted by TargetScan and identified by Dual luciferase reporter gene assay. Results: MiRNA-210 was overexpressed in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells ( P < 0.05). Silencing of miRNA-210 inhibited the viability and promoted the apoptosis of HepG2 and HepG2.2.15 cells ( P < 0.05). EGR3 was a target of miRNA-210, which was down-regulated in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells ( P < 0.05). Silencing of miRNA-210 increased the mRNA and protein expression of EGR3 ( P < 0.05). Silencing of EGR3 reversed the anti-tumor effect of miRNA-210 inhibitor on HepG2 and HepG2.2.15 cells ( P < 0.05). Conclusions: Silencing of miRNA-210 inhibits the progression of liver cancer and HBV-associated liver cancer via up-regulating EGR3.
MiRNAs might function as oncogenes or tumor suppressor genes in the tumorigenesis process. Dysregulation of miR-345 is a frequent event in many types of human cancers. However, the tissue miR-345 expression level in non-small cell lung cancer (NSCLC) and its potential clinical significance remains unknown.Real-time PCR was conducted to evaluate the expression level of miR-345 in NSCLC tissues as well as cell lines. Then the association between tissue miR-345 expression level and clinical outcome was investigated.The expression level of miR-345 was significantly decreased in NSCLC tissues and cell lines compared with the controls (P<0.05; P<0.01). Tissue miR-345 expression level was associated with various clinicopathological parameters including LN metastasis (P=0.012), distant metastasis (P=0.007), TNM stage (P=0.008) and grade (P=0.030). In addition, the NSCLC patients in thelow tissue miR-345 expression group had significantly shorter 5-year overall survival time than those in the high tissue miR-345expression group (P=0.016). Multivariate analysis showed that tissue miR-345 was an independent risk factor for NSCLC (HR=3.921, 95% CI: 2.285-10.540; P=0.008).The expression level of miR-345 was reduced in NSCLC tissues and cell lines. Low tissue miR-345 expression was associated with progression and poor prognosis of NSCLC, indicating that tissue miR-345 may serve as a novel prognostic marker in NSCLC.
The occurrence of root rot of tobacco (Nicotiana tobacum L.) was observed in the fields of Xianchengxian, China. The symptoms showed as plant wilt, leaves chlorosis and root necrosis. The isolated fungus was identified as Fusarium sacchari by the morphological characteristics and molecular identification of translation elongation factor 1-alpha (EF-1α), the RNA polymerase II largest subunit (RPB1) and second largest subunit (RPB2) gene sequences. Phylogenetic analysis of the concatenated three-loci of EF-1α, RPB1 and RPB2 showed that the isolate was placed in the F. sacchari group. The pathogenicity test showed that F. sacchari cause root rot of tobacco. This is the first report of F. sacchari causing root rot of tobacco in China.
Saccharina japonica is a brown macroalga that has been commercially cultivated in China for almost a century. As a natural raw material, it is widely used in the food and pharmaceutical industries, and it may potentially be useful for biofuel production. However, little is known about the genes involved in carbohydrate biosynthesis, and their regulation is less understood. In this study, the analysis of growth traits and alginate and mannitol contents suggested that sporophyte development could be divided into four stages. Accordingly, we performed transcriptome analysis of the S. japonica sporophyte. In total, 589 million clean reads were generated, and 4,514 novel genes were identified. Gene expression analysis revealed that 2,542 genes were differentially expressed. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis indicated that these genes were significantly enriched in “Carbon metabolism,” “Photosynthesis,” and “Photosynthesis‐antenna proteins” pathways, which are important for metabolism of various carbohydrates during sporophyte development. Systematic analysis identified the genes encoding enzymes for the biosynthesis of cell wall carbohydrates (including alginate, fucoidan, and cellulose) and cytoplasm storage carbohydrates (mannitol, laminarin, and trehalose). Among them, some key genes associated with carbohydrate content were further identified based on detailed expression profiling, representing good candidates for further functional studies. This study provides a global view of the carbohydrate metabolism process and an important resource for functional genomics studies in S. japonica . The results obtained lay the basis for elucidating the molecular mechanism of carbohydrate biosynthesis and for genetic breeding of carbohydrates‐related traits in kelp.
// Jianzhou Tang 1, 5, * , Hui Li 2, * , Jiashun Luo 3 , Hua Mei 4 , Liang Peng 1 , Xiaojie Li 5 1 Department of Biological and Environmental Engineering, Changsha University, Changsha 410003, Hunan, China 2 Department of Microbiology and Immunology, Medical School of Jishou University, Jishou 416000, Hunan, China 3 Institute of Medical Sciences, Medical School of Jishou University, Jishou 416000, Hunan, China 4 Hunan Guangxiu Hospital, Changsha 410002, Hunan, China 5 College of Animal Science and Technology of Hunan Agriculture University, Changsha 410128, Hunan, China * These authors contributed equally to this work and should be considered as co-first authors Correspondence to: Jianzhou Tang, email: Z20050711@ccsu.edu.cn Keywords: LSP1, breast cancer, risk, meta-analysis Received: June 06, 2016 Accepted: August 26, 2016 Published: August 31, 2016 ABSTRACT The association between the LSP1 rs3817198 T > C polymorphism and breast cancer risk has been widely investigated, but remains controversial. We therefore undertook a comprehensive meta-analysis to provide a high-quality evaluation of this association. A literature search was performed among Pubmed, EMBASE and Chinese National Knowledge Infrastructure (CNKI) databases prior to July 31, 2016, and the strength of the association between the LSP1 rs3817198 T > C polymorphism and breast cancer risk was assessed based on odds ratio (OR) and 95% confidence interval (95% CI). In total, 12 studies with 50,525 cases and 54,302 controls were included. Pooled risk estimates indicated a significant association between the LSP1 rs3817198 T > C polymorphism and breast cancer risk. Analysis of cases stratified based on ethnicity suggested that the association was significant in both Caucasian and Asian populations. Stratification based on source of controls revealed an association only in population-based studies. These findings indicate the LSP1 rs3817198 T > C polymorphism is associated with increased risk of breast cancer, especially in Caucasian and Asian populations. Large, well-designed studies with different ethnicities are still needed to verify our findings.
Coronary artery disease (CAD) is one of the main causes of hospitalization worldwide and has high morbidity. MicroRNAs (miRNAs) play an important role in the pathogenesis of cardiovascular diseases. miR-451 is a special miRNA that is involved in many cancers' development. At present, there is no research about miR-451 in coronary heart disease. In this study, we aimed to identify the action mechanism of miR-451 in coronary heart disease and human umbilical vein endothelial cells (HUVECs). In this study, we found that miR-451 is up-regulated in the peripheral blood of patients with coronary heart disease. Moreover, TargetScan and dual-luciferase reporter gene assay results showed that VEGFA is a direct target gene of miR-451. C (CCK-8) and flow cytometry assay results showed that miR-451 mimic significantly inhibits cell proliferation and promotes apoptosis in HUVECs. Moreover, we found that the role of miR-451 in HUVECs is associated with the PI3K-Akt-mTOR pathway. Taken together, the data indicates that miR-451 might be a novel bio-marker for coronary heart disease.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)