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MAPK/p38 regulation of cytoskeleton rearrangement accelerates induction of macrophage activation by TLR4, but not TLR3
Bian, HJ;Li, FF;Wang, WW;Zhao, Q;Gao, SS;Ma, JC;Li, X;Ren, WH;Qin, CY;Qi, JN
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 2017年 40卷5期 页码:1495-1503
IFN-BETA PRODUCTION; ACTIN CYTOSKELETON; IN-VIVO; CELLS; REORGANIZATION; RECOGNITION; VINCRISTINE; INHIBITION; ENDOTOXIN; LEUKEMIA
Toll-like receptor 3 (TLR3) and TLR4 utilize adaptor proteins to activate mitogen-activated protein kinase (MAPK), resulting in the acute but transient inflammatory response aimed at the clearance of pathogens. In the present study, it was demonstrated that macrophage activation by lipopolysaccharide (LPS) or poly(I:C), leading to changes in cell morphology, differed significantly between the mouse macrophage cell line RAW264.7 and mouse primary peritoneal macrophages. Moreover, the expression of alpha- and beta-tubulin was markedly decreased following LPS stimulation. By contrast, alpha- and beta-tubulin expression were only mildly increased following poly(I:C) treatment. However, the expression of beta-actin and GAPDH was not significantly affected. Furthermore, it was verified that vincristine pretreatment abrogated the cytoskeleton rearrangement and decreased the synthesis and secretion of proinflammatory cytokines and migration of macrophages caused by LPS. Finally, it was observed that the MAPK/p38 signaling pathway regulating cytoskeleton rearrangement may participate in LPS-induced macrophage cytokine production and migration. Overall, the findings of the present study indicated that MAPK/p38 regulation of the cytoskeleton, particularly tubulin proteins, plays an important role in LPS-induced inflammatory responses via alleviating the synthesis and secretion of proinflammatory cytokines and inhibiting the migration of macrophages.
Cardioprotective effect of nicorandil against myocardial injury following cardiac arrest in swine
Liang, LN;Zhong, X;Zhou, Y;Hou, ZQ;Hu, HR;Zhu, FF;Chen, JB;Ji, XF;Shang, DY
AMERICAN JOURNAL OF EMERGENCY MEDICINE 2017年 35卷8期 页码:1082-1089
K-ATP CHANNELS; CARDIOPULMONARY-RESUSCITATION; VENTRICULAR-FIBRILLATION; ARTERIAL-HYPOTENSION; DYSFUNCTION; HEART
Introduction: Nicorandil, a vasodilatory drug used to treat angina, was reported to protect against myocardial ischemia- reperfusion injury in various animal models. However, its cardioprotective action following cardiac arrest is unknown. We examined the cardioprotective effects of nicorandil in a porcine model of cardiac arrest and resuscitation.;-;Methods: Ventricular fibrillation was induced electrically for 4 min in anesthetized domestic swine, followed by cardiopulmonary resuscitation. Sixteen successfully resuscitated animals were randomized to saline control (n = 8) or nicorandil (n = 8) groups. Nicorandil (150 mu g/kg) was administered by central intravenous injection at onset of restoration of spontaneous circulation (ROSC), followed by 3 mu g/kg/min infusion until reperfusion end. Sham-operated animals received surgery only (n = 4). Hemodynamic parameters weremonitored continuously. Blood samples were taken at baseline, 5, 30, 180, and 360 min after ROSC. Left ventricular ejection fraction was assessed by echocardiography at baseline and 6 h after ROSC. The animals were euthanized 6 h after ROSC, and the cardiac tissue was removed for analysis.;-;Results: 6 h after ROSC, nicorandil had significantly improved all hemodynamic variables (all P < 0.05) except the maximum rate of left ventricular pressure decline and heart rate (P > 0.05) compared with the control group. Control animals showed elevated cardiac troponin I and lactate levels compared with sham animals, which were significantly decreased following nicorandil treatment (P < 0.05). In the saline control group, the adenosine triphosphate (ATP) content was largely reduced but subsequently rescued by nicorandil (P < 0.05). Histopathologic injurywas reducedwith nicorandil treatment. Nicorandil reduced cardiomyocyte apoptosis as evidenced by reduced terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells, decreased Bax and caspase-3 expression, and increased Bcl-2 expression in the myocardium (all P < 0.05).;-;Conclusion: Nicorandil exhibited cardioprotective effects on myocardial injury following cardiac arrest via improvement in post-resuscitationmyocardial dysfunction and energymetabolism, reduction inmyocardial histopathologic injury, and antiapoptotic effects. (C) 2017 Elsevier Inc. All rights reserved.
Photoelectrochemical Cytosensing of RAW264.7 Macrophage Cells Based on a TiO2 Nanoneedls@MoO3 Array
Pang, XH;Bian, HJ;Su, MH;Ren, YY;Qi, JN;Ma, HM;Wu, D;Hu, LH;Du, B;Wei, Q
ANALYTICAL CHEMISTRY 2017年 89卷15期 页码:7950-7957
LIGHT PHOTOCATALYTIC ACTIVITY; LITHIUM-ION BATTERIES; ALKALINE-PHOSPHATASE; HIGH-ENERGY; THIN-FILMS; NANOTUBES; IMMUNOASSAY; NANOPARTICLES; ANTIBODIES; ELECTRODE
We have developed a photoelectrochemical (PEC) cytosensor for ultrasensitive detection of RAW264.7 cells by the signal change of a TiO2 nanoneedles (NNs)@MoO3 array. For the first time, a TiO2 NNs@ MoO3 array was adopted for the fabrication of the cytosensor for the signal output. The well-matched alignment of TiO2 NNs and MoO3 efficiently suppresses the recombination of photogenerated electron and hole (e(-)/h(+)) pairs for improved photon-to-current conversion efficiency. The RAW264.7 cell and F4/80 antibody could form the biocomplexes because of the specific recognition between each other. The constructed PEC cytosensor based on the TiO2 NNs@MoO3 array displayed good PEC property for detection of RAW264.7 cells. The numbers of RAW264.7 cells are directly detected through the decrement of photocurrent intensity, due to the increased steric hindrance when RAW264.7 cells are captured. The PEC cytosensor showed an ultrasensitive response to RAW264.7 cells with a linear range of 50-15 000 cells/mL and a detection limit of 50 cells/mL. The designed cytosensor based on a TiO2 NNs@MoO3 array offers an ideal platform to detect RAW264.7 cells with excellent stability, reproducibility, and selectivity and served as a model for the fabrication of cytosensors for other cells.
Rho-kinase signaling pathway promotes the expression of PARP to accelerate cardiomyocyte apoptosis in ischemia/reperfusion
Bian, HJ;Zhou, Y;Yu, B;Shang, DY;Liu, FL;Li, B;Qi, JN
MOLECULAR MEDICINE REPORTS 2017年 16卷2期 页码:2002-2008
MEDIATED AIF TRANSLOCATION; POLY(ADP-RIBOSE) POLYMERASE-1; REPERFUSION; INHIBITION; INJURY; CELLS; RAT
It has been previously reported that Rho-kinase (ROCK) and poly ADP-ribose polymerase (PARP) serve critical roles in myocardial ischemia/reperfusion (I/R) injury. Studies have additionally demonstrated that the activation of ROCK and the expression of PARP are increased in I/R. However, the effect and mechanism of the two proteins remains to be fully elucidated in I/R. In addition, whether they can be influenced by each other is unclear. In the present study, it was demonstrated that ischemia followed by reperfusion resulted in a significant increase in ROCK and PARP. In addition, Y-27632 (ROCK inhibitor) and 3-aminobenzamide (3-AB; PARP inhibitor) pretreatment rescued myocardial infarction size and cardiomyocyte apoptosis. The inhibitory role of Y-27632 was observed to be superior to that of the 3-AB group. In addition, Y-27632 and 3-AB diminished extracellular signal-related kinase (ERK) phosphorylation and the production of tumor necrosis factor a and interleukin 6. Overall, the results of the present study suggested that the inhibition of ROCK leads to reduced myocardial infarction size and cardiomyocyte apoptosis via the PARP/ERK signaling pathway.
KLF15 protects against isoproterenol-induced cardiac hypertrophy via regulation of cell death and inhibition of Akt/mTOR signaling
Gao, L;Guo, YD;Liu, XF;Shang, DY;Du, YJ
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2017年 487卷1期 页码:22-27
TRANSCRIPTION FACTOR KLF5; KRUPPEL-LIKE FACTORS; ANGIOTENSIN-II; EXPRESSION; ACTIVATION; DIFFERENTIATION; KLF5/BTEB2; FIBROSIS
Increasing evidence indicate that the Kruppel-like factor KLF15, a member of Cys2/His2 zinc-finger DNA-binding proteins, attenuates cardiac hypertrophy. However, the role of KLF15 in cardiovascular system is largely unknown and the exact molecular mechanism of its protective function is not fully elucidated. In the present study, we established a mouse model of cardiac hypertrophy and found that KLF15 expression was down-regulated in hypertrophic hearts. To evaluate the roles of KLF15 in cardiac hypertrophy, we generated transgenic mice overexpressing KLF15 of KLF15 knockdown mice and subsequently induced cardiac hypertrophy. The results indicated that KLF15 overexpression protects mice from ISO-induced cardiac hypertrophy, with reduced ratios of heart weight (HW)/body weight (BW) and cross-sectional area. We also observed that KLF15 overexpression attenuated cardiac fibrosis, inhibited apoptosis and induced autophagy in cardiomyocytes compared with KLF15 knockdown mice. More importantly, we found that the KLF15 overexpression inhibited the Akt/mTOR signaling pathway. Taken together, our findings imply that KLF15 possesses potential anti-hypertrophic and anti-fibrotic functions, possibly via regulation of cell death pathways and the inhibition of Akt/mTOR axis. KLF15 may constitute an efficient candidate drug for the treatment of heart failure and other cardiovascular diseases. (C) 2017 Elsevier Inc. All rights reserved.
A bio-chemical application of N-GQDs and g-C3N4 QDs sensitized TiO2 nanopillars for the quantitative detection of pcDNA3-HBV
Pang, XH;Bian, HJ;Wang, WJ;Liu, C;Khan, MS;Wang, Q;Qi, JN;Wei, Q;Du, B
BIOSENSORS & BIOELECTRONICS 2017年 91卷 页码:456-464
GRAPHENE QUANTUM DOTS; CARBON NITRIDE NANOSHEET; HYDROGEN EVOLUTION; GRAPHITIC C3N4; DEGRADATION; PHOTOCATALYSTS; PERFORMANCE; ELECTRODES; EFFICIENCY; CONVERSION
Herein, TiO2 nanopillars (NPs)/N-doped graphene quantum dots (N-GQDs)/g-C3N4 QDs heterojunction efficiently suppressed the photogenerated charges recombination and improved photo-to-current conversion efficiency. The introduced N-GQDs and g-C3N4 QDs could result in more effective separation of the photogenerated charges, and thus produce a further increase of the photocurrent. TiO2 NPs/N-GQDs/g-C3N4 QDs were firstly applied as the photoactive materials for the fabrication of the biosensors, and the primers of pcDNA3-HBV were then adsorbed on the TiO2 NPs/N-GQDs/g-C3N4 QDs modified electrode under the activation of EDC/NHS. With increase of the pcDNA3-HBV concentration, the photocurrent reduced once the double helix between the primers and pcDNA3-HBV formed. The developed photoelectrochemical (PEC) biosensor showed a sensitive response to pcDNA3-HBV in a linear range of 0.01 fmol/L to 20 nmol/L with a detection limit of 0.005 fmol/L under the optimal conditions. The biosensor exhibited high sensitivity, good selectivity, good stability and reproducibility.
Effect of atorvastatin on serum omentin-1 in patients with coronary artery disease
Chen, QQ;Shang, XC;Yuan, M;Liang, LN;Zhong, X
CORONARY ARTERY DISEASE 2017年 28卷1期 页码:44-51
POLYCYSTIC-OVARY-SYNDROME; TYPE-2 DIABETES-MELLITUS; METABOLIC SYNDROME; ADIPOSE-TISSUE; CARDIOVASCULAR-DISEASE; HYPERCHOLESTEROLEMIC PATIENTS; ENDOTHELIAL DYSFUNCTION; MYOCARDIAL-INFARCTION; INSULIN SENSITIVITY; GLUCOSE-TOLERANCE
Objective An association between coronary artery disease (CAD) and serum omentin-1 was recently identified. The aim of the present study was to investigate the effect of atorvastatin on serum levels of omentin-1 in patients with CAD.;-;Methods One-hundred and ninety-eight patients with CAD were divided into two groups: those with acute coronary syndrome (ACS) and those with stable angina pectoris (SAP). All patients were randomized to receive atorvastatin therapy at a dose of either 20 or 40 mg/day for 12 weeks. Serum omentin-1 levels and other parameters were determined at baseline and at the end of the study.;-;Results Atorvastatin at 20 and 40 mg/day increased serum omentin-1 levels in patients with ACS (20 mg, P = 0.007; 40 mg, P < 0.001) and in those with SAP (20 mg, P = 0.017; 40 mg, P < 0.001). Atorvastatin at 40 mg induced greater changes in serum omentin-1 levels compared with 20 mg atorvastatin in both the ACS group (P = 0.003) and the SAP group (P = 0.012). The increments of serum omentin-1 levels with atorvastatin administration inversely correlated with changes in LDL cholesterol (r = -0.145, P = 0.041), interleukin-6 (r = -0.162, P = 0.023), and high-sensitivity C-reactive protein (r = -0.185, P = 0.009) in patients with CAD. Furthermore, changes in LDL cholesterol (beta = -0.158, P = 0.027) and interleukin-6 (beta = -0.154, P = 0.044) remained independent determinants of omentin-1 alterations in standard multiple regression analysis (R-2 = 0.122, P = 0.006) after adjusting for age, sex, smoking, family history of CAD, and BMI in patients with CAD.;-;Conclusion Atorvastatin increased serum omentin-1 concentrations in patients with CAD in a dose-dependent manner. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.
Spleen Stiffness Is Superior to Liver Stiffness for Predicting Esophageal Varices in Chronic Liver Disease: A Meta-Analysis
Ma, XW;Wang, L;Wu, H;Feng, YM;Han, XB;Bu, HR;Zhu, Q
PLOS ONE 2016年 11卷11期 影响因子:3.057
SIGNIFICANT PORTAL-HYPERTENSION; TRANSIENT ELASTOGRAPHY; GASTROESOPHAGEAL VARICES; DIAGNOSTIC-ACCURACY; CIRRHOTIC-PATIENTS; SHEAR-WAVE; NONINVASIVE ASSESSMENT; ARFI ELASTOGRAPHY; HEPATITIS; RISK
Background and Aims;-;Liver stiffness (LS) and spleen stiffness (SS) are two most widely accessible non-invasive parameters for predicting esophageal varices (EV), but the reported accuracy of the two predictors have been inconsistent across studies. This meta-analysis aims to evaluate the diagnostic performance of LS and SS measurement for detecting EV in patients with chronic liver disease (CLD), and compare their accuracy.;-;Methods;-;Pubmed/Medline, Embase, Cochrane Library and Ovid were searched for all studies assessing SS and LS simultaneously in EV diagnosis. A total of 16 studies including 1892 patients were included in this meta-analysis, and the pooled statistical parameters were calculated using the bivariate mixed effects models.;-;Results;-;In detection of any EV, for LS measurement, the summary sensitivity was 0.83 (95% confidence interval [CI]: 0.78-0.87), and the specificity was 0.66 (95% CI: 0.60-0.72). While for SS measurement, the pooled sensitivity and specificity was 0.88 (95% CI: 0.83-0.92) and 0.78 (95% CI: 0.73-0.83). The summary receiver operating characteristic (SROC) curve values of LS and SS were 0.81 (95% CI: 0.77-0.84) and 0.88 (95% CI: 0.85-0.91) respectively, and the results had statistical significance (P<0.01). The diagnostic odds ratio (DOR) of SS (25.73) was significantly higher than that of LS (9.54), with the relative DOR value was 2.48 (95% CI: 1.10-5.60), P<0.05.;-;Conclusions;-;Under current techniques, SS is significantly superior to LS for identifying the presence of EV in patients with CLD. SS measurement may help to select patients for endoscopic screening.
Metabolomics of papillary thyroid carcinoma tissues: potential biomarkers for diagnosis and promising targets for therapy
Shang, XC;Zhong, X;Tian, XS
TUMOR BIOLOGY 2016年 37卷8期 页码:11163-11175
MAGNETIC-RESONANCE-SPECTROSCOPY; MASS-SPECTROMETRY; CANCER CELLS; EXPRESSION; METABOLITES; MELATONIN; DISEASE; SAMPLES; GC/MS; ACID
Papillary thyroid carcinoma (PTC) is the most common pathological type of thyroid cancer. Our study was to construct a tissue-targeted metabolomics analysis method based on untargeted and targeted metabolic multi-platforms to identify a comprehensive PTC metabolic network in clinical samples. We applied untargeted gas chromatography-time-of-flight mass spectrometry (GC-TOF-MS) for preliminary screening of potential biomarkers. With diagnostic models constructed using principal component analysis (PCA), partial least squares discriminant analysis (PLS-DA) and orthogonal partial least squares discriminant analysis (OPLS-DA), 45 differentially abundant metabolites with a variable importance in the projection (VIP) value greater than 1 and a P value less than 0.05 were identified, and we show that our approach was able to discriminate PTC tissues from healthy tissues. We then performed validation experiments based on targeted GC-TOF-MS combined with ultra-high-performance liquid chromatography-triple-quadrupole mass spectrometry (UHPLC-QqQ-MS) through constructing linear standard curves of analytes. Ultimately, galactinol, melibiose, and melatonin were validated as significantly altered metabolites (p < 0.05). These three metabolites were defined as a combinatorial biomarker to assist needle biopsy for PTC diagnosis as demonstrated by receiver operating characteristic (ROC) curve analysis, which revealed an area under the ROC curve (AUC) value of 0.96. Based on the metabolite enrichment analysis results, the galactose metabolism pathway was regarded as an important factor influencing PTC development by affecting energy metabolism. Alpha-galactosidase (GLA) was considered to be a potential target for PTC therapy.
MiR-130b inhibits proliferation and induces apoptosis of gastric cancer cells via CYLD
Sun, BY;Li, L;Ma, WD;Wang, SK;Huang, CJ
TUMOR BIOLOGY 2016年 37卷6期 页码:7981-7987
DOWN-REGULATION; DEUBIQUITINASE CYLD; BREAST-CANCER; METASTASIS; GROWTH; OSTEOSARCOMA; MMP7; PHOSPHORYLATION; INFLAMMATION; ACTIVATION
A role of microRNA-130b (miR-130b) in the carcinogenesis of gastric cancer remains undetermined. In this study, we studied the effects and mechanism of miR-130b to the gastric cell proliferation and apoptosis. We found that the levels of miR-130b significantly up-regulated in gastric cancer tissue, compared to the paired adjacent non-tumor gastric tissue. The miR-130b levels in gastric cancer cell lines were significantly higher than those in control normal gastric tissues. Transfection with the miR-130b mimic enhanced the cell proliferation and suppressed cell apoptosis in gastric cancer cells, while transfection with the anti-sense of miR-130b (anti-miR-130b) suppressed cell proliferation and induced cell apoptosis in gastric cancer cells. Bioinformatics analyses showed that cylindromatosis gene (CYLD) was a potential target gene of miR-130b. The luciferase activity assay and western blot verified that miR-130b targeted CYLD messenger RNA (mRNA) to modulate its protein levels. Together, our study suggests that aberrantly expressed miR-130b may regulate cell apoptosis and proliferation of human gastric cancer cells via CYLD, which appears to be a promising therapeutic target for gastric cancer.
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