Time filter

Source Type

Xiong Y.,Jilin University | Xiong Y.,Beihua University | Tan Y.,Jilin University | Tan Y.,Jilin Province Peoples Hospital | Song Y.G.,Beihua University
Hepatitis Monthly | Year: 2014

Background: The hepatitis B virus (HBV) antigen-induced cellular immune response plays an important role in HBV clearance. Changes in the diversity of complementarity determining region 3 (CDR3) and T-cell receptor (TCR) sequences are used to monitor the response of T cells to antigens. Objectives: The aim of the present study was to determine whether the TCR Vβ repertoire of patients with chronic severe hepatitis B (CSHB) undergoes increased stimulation, and to identify conserved motifs in specific TCR Vβ families. Patients and Methods: Peripheral blood mononuclear cells (PBMCs) from 18 patients with CSHB were sorted into CD4+ and CD8+ T subsets, using monoclonal antibody-coated magnetic beads. The TCR Vβ CDR3 was subsequently characterized using immune spectratyping. The TCR Vβ families exhibiting a CDR3 spectratype that underwent monoclonal expansion were sequenced. Results: The number of oligoclonal or monoclonal expansion TCR Vβ families detected in the analyzed CD8+ T cells was significantly higher than the number detected in CD4+ T cells. The CDR3 spectratype analysis showed predominant usage of TCR Vβ5, Vβ7, Vβ9, Vβ12, and Vβ18 families in CD8+ T cell subsets of CSHB patients. Furthermore, conserved amino acid motifs were found to be associated with the monoclonal expansion of CD8+ TCR Vβ families. In addition, JB1S1 and JB2S7 region genes were present at a high frequency. Conclusions: The CD4+ and CD8+ TCR Vβ gene families undergo clonal expansion in CSHB patients, and CD8+ T cells play a major role in the pathogenesis of CSHB. Moreover, the conserved motifs and limited use of joining region genes observed in the CSHB patients of this cohort indicated that similar antigenic epitopes are recognized. © 2014, Kowsar Corp.

Liu X.,Jilin University | Pei C.,Jilin Province Peoples Hospital | Yan S.,Jilin Province Cancer Hospital | Liu G.,Jilin University | And 4 more authors.
Tumor Biology | Year: 2015

Recent evidence demonstrated an enhanced metastasis of non-small cell lung cancer (NSCLC) cells induced by lipopolysaccharide (LPS) stimulation, which reflected an important role of inflammation in tumor progression. However, the underlying mechanisms still remain unclear. Here, we evaluated the potential role of reactive oxygen species (ROS) in Toll-like receptor 4 (TLR4) signaling enhanced NSCLC metastasis. NSCLC cells were isolated from clinical surgical tissues. We found that LPS stimulation of NSCLC cells facilitates their metastasis that was accompanied by increased ROS production and could be abrogated by ROS inhibition. NADPH oxidase was essential for TLR4 signaling-enhanced NSCLC metastasis. Elevated NADPH oxidase 1 (NOX1) expression by LPS stimulation was observed. Blockade of NOX1 with ML171 alleviated enhanced NSCLC metastasis by TLR4 signaling. Enforced NOX1 expression promoted TLR4 signaling-enhanced NSCLC metastasis, while decreased NOX1 expression inhibited TLR4 signaling-enhanced NSCLC metastasis. Further, NOX1 could regulate the expression of CXCR4 and matrix metallopeptidase 9 (MMP9) in NSCLC cells. NOX1 expression in tumor tissues was correlated with TLR4 expression and clinical stages in NSCLC patients. Finally, inhibition of NOX1/ROS prevented enhanced lung tumor burdens of NSCLC by LPS-induced acute lung infection. Our findings demonstrated a crucial role of NOX1-dependent ROS for TLR4 signaling to enhance the metastasis of NSCLC, which could further the understanding of NSCLC pathogenesis and helpful for developing novel therapeutics for NSCLC. © 2015, International Society of Oncology and BioMarkers (ISOBM).

Du J.,Jilin University | Li Z.,Jilin Province Peoples Hospital | Shi J.,Jilin University | Bi L.,Jilin University
Journal of International Medical Research | Year: 2014

Objective: To analyse the association between serum interleukin (IL)-23 mRNA levels and clinical characteristics in patients with systemic lupus erythematosus (SLE).Methods: Serum IL-23 and IL-17 mRNA levels were quantified using real-time reverse transcription-polymerase chain reaction in patients with SLE and healthy controls. Disease activity was assessed using the SLE Disease Activity Index-2k.Results: A total of 108 patients with SLE and 60 control subjects were recruited. IL-23 mRNA levels were significantly higher in patients with SLE compared with healthy controls, and in patients with SLE and renal involvement compared with SLE alone. IL-23 mRNA levels were not different between patients with active or inactive SLE, but the IL-17/IL-23 ratio was significantly higher in patients with active disease. IL-17 and IL-23 mRNA levels were strongly correlated.Conclusions: Serum IL-23 mRNA was elevated in patients with SLE and renal disease, and the IL-17/IL-23 ratio was higher in patients with active SLE. These findings suggest that IL-23 may play an important role in SLE pathogenesis, and that the IL-17/IL-23 ratio may be useful biomarker for active disease. © The Author(s) 2014.

Li B.,Jilin University | Li B.,Jilin Province Peoples Hospital | Li B.,University of Louisville | Liu S.,Jilin Province Peoples Hospital | And 2 more authors.
Experimental Diabetes Research | Year: 2012

Diabetic cardiomyopathy and nephropathy are two major causes of death of patients with diabetes. Extra generation of reactive oxygen species (ROS), induced by hyperglycemia, is considered as the main reason for the development of these diabetic complications. Transcription factor, NFE2-related factor 2 (Nrf2), is a master regulator of cellular detoxification response and redox status, and also provides a protective action from various oxidative stresses and damages. Recently we have demonstrated its important role in determining the susceptibility of cells or tissues to diabetes-induced oxidative stress and/or damage. Therefore, this review will specifically summarize the information available regarding the effect of Nrf2 on the diabetic complications with a focus on diabetic cardiomyopathy and nephropathy. Given the feature that Nrf2 is easily induced by several compounds, we also discussed the role of different Nrf2 activators in the prevention or therapy of various diabetic complications. These findings suggest that Nrf2 has a potential application in the clinic setting for diabetic patients in the short future. Copyright © 2012 Bing Li et al.

Lian J.-H.,Jilin University | Lian J.-H.,Jilin Province Peoples Hospital | Wang W.-H.,Jilin University | Wang J.-Q.,Jilin Province Peoples Hospital | And 2 more authors.
Asian Pacific Journal of Cancer Prevention | Year: 2013

Objective: MicroRNAs (miRNAs) are a small class of non-coding, single-stranded RNAs with a critical role in genesis and maintenance of renal cancer mainly through binding to 3'-untranslated regions (3'UTR) of target mRNAs, which causes a block of translation and/or mRNA degradation. The aim of the present study was to investigate the potential effects of miR-122 in human renal cell carcinomas. Methods: The expression level of miR-122 was quantified by qRT-PCR. MTT, colony formation, invasion and migration assays were used to explore the potential functions of miR-122 in human renal cell carcinoma cells. Results: Cellular growth, invasion and migration in two A498 and 786-O cells were significantly increased after miR-122 transfection. Further experiments demonstrated that overexpression of miR-122 resulted in the increase of phospho-Akt (Ser473) and phospho-mTOR (Ser2448), then activation of mTOR targets, p70S6K and 4E-BP1. Conclusions: The up-regulation of miR-122 may play an important role in the progress of renal cancer through activating PI3K/Akt signal pathway and could be a potential molecular target for anti-cancer therapeutics.

Wang Y.,Jilin University | Wang Y.,Jilin Province Peoples Hospital | Zhang R.,Jilin University | Wu D.,Jilin University | And 5 more authors.
Journal of Experimental and Clinical Cancer Research | Year: 2013

Background: MYST1 (also known as hMOF), a member of the MYST family of histone acetyltransferases (HATs) as an epigenetic mark of active genes, is mainly responsible for histone H4K16 acetylation in the cells. Recent studies have shown that the abnormal gene expression of hMOF is involved in certain primary cancers. Here we examined the involvement of hMOF expression and histone H4K16 acetylation in primary renal cell carcinoma (RCC). Simultaneously, we investigated the correlation between the expression of hMOF and clear cell RCC (ccRCC) biomarker carbohydrase IX (CA9) in RCC. Materials and methods. The frozen RCC tissues and RCC cell lines as materials, the reverse transcription polymerase chain reaction (RT-PCR), western blotting and immunohistochemical staining approaches were used. Results: RT-PCR results indicate that hMOF gene expression levels frequently downregulated in 90.5% of patients (19/21) with RCC. The reduction of hMOF protein in both RCC tissues and RCC cell lines is tightly correlated with acetylation of histone H4K16. In addition, overexpression of CA9 was detected in 100% of ccRCC patients (21/21). However, transient transfection of hMOF in ccRCC 786-0 cells did not affect both the gene and protein expression of CA9. Conclusion: hMOF as an acetyltransferase of H4K16 might be involved in the pathogenesis of kidney cancer, and this epigenetic changes might be a new CA9-independent RCC diagnostic maker. © 2013 Wang et al.; licensee BioMed Central Ltd.

Yuan G.,Jilin University | Qi B.,Jilin Province Peoples Hospital | Luo Q.,Jilin University
International Journal of Clinical and Experimental Medicine | Year: 2016

Cerebrovascular autoregulation maintains brain hemostasis via regulating cerebral flow when blood pressure fluctuation occurs. Monitoring autoregulation can be achieved by transcranial Doppler ultrasonography, the pressure reactivity index (PRx) can serve as a secondary index of vascular deterioration, and outcome and prognosis are assessed by the low-frequency PRx. Although great changes in arterial blood pressure (ABP) occur, complex neurogenic, myogenic, endothelial, and metabolic mechanisms are involved to maintain the flow within its narrow limits. The steady association between ABP and cerebral blood flow (CBF) reflects static cerebral autoregulation (CA). Spreading depolarization (SD) is a sustained depolarization of neurons with concomitant pronounced breakdown of ion gradients, which originates in patients with brain ischemia, hemorrhage, trauma, and migraine. It is characterized by the propagation of an extracellular negative potential, followed by an increase in O2 and glucose consumption. Immediately after SD, CA is transiently impaired but is restored after 35 min. This process initiates a cascade of pathophysiological mechanisms, leading to neuronal damage and loss if consecutive events are evoked. The clinical application of CA in regulating CBF is to dilate the cerebral arteries as a compensatory mechanism during low blood pressure, thus protecting the brain from ischemia. However, transient impairment of CBF autoregulation due to the mechanism regulated by SD autoregulation has not been reported previously. In this review, we found that SD serves as a vital factor that disrupts CBF autoregulation, and these findings provide insight into the mechanical complexities of SD-induced autoregulatory failure. © 2016, E-Century Publishing Corporation. All rights reserved.

Mi C.,Yanbian University | Shi H.,Yanbian University | Ma J.,Yanbian University | Han L.Z.,Jilin Province Peoples Hospital | And 2 more authors.
Oncology Reports | Year: 2014

Celastrol is a quinone methide triterpene derived from Tripterygium wilfordii Hook F., a plant used in traditional medicine. In the present study, we reported that celastrol potentiated tumor necrosis factor-α (TNF-α)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). In addition, celastrol significantly reduced the invasion of MDA-MB-231 human breast cancer cells after TNF-α stimulation. As matrix metalloproteinase-9 (MMP-9) plays a critical role in tumor metastasis, we analyzed its expression with celastrol treatment. Western blot analysis and real-time PCR showed that celastrol dose-dependently suppressed TNF-α-induced MMP-9 gene expression at both the mRNA and protein levels in MDA-MB-231 cells. Taken together, our findings indicate that celastrol may be a potential candidate for breast cancer chemotherapy.

Lu W.,Jilin Province Peoples Hospital | Du S.,Jilin Province Peoples Hospital | Wang J.,Jilin Province Peoples Hospital
Molecular Medicine Reports | Year: 2015

Prostate cancer is the second most common disease of the male reproductive system. Berberine is a quaternary ammonium salt that is extracted from plants. The aim of the current study was to explore the antitumor activity of berberine in prostate cancer cells and identify the underlying mechanism of its effects. PC3 human and RM-1 mouse prostate cancer cells were treated with increasing concentrations of berberine, followed by analysis of the cell viability with an MTT assay. The results demonstrated that berberine markedly inhibited the proliferation of PC3 and RM-1 cells, and that the inhibitory effects to PC3 and RM-1 were enhanced in a concentration- and time-dependent manner. Flow cytometry was used to analyze the cell cycle of PC3 human prostate cancer cells, and the results demonstrated that G0/G1 phase arrest was induced following treatment with 10 μM berberine (P<0.05). However, with an increased concentration of berberine (50 μM) the survival rate of PC3 cells at the G2/M phase was significantly increased compared with the cells treated with 10 μM berberine, which suggests that different cell cycle signaling pathways were activated when PC3 cells were treated with low and high concentrations of berberine. Thus, clarifying the mechanism underlying these effects in prostate cancer may provide novel molecular targets for prostate cancer therapy.

Zhang L.-H.,Jilin province peoples hospital | Li L.,Jilin province peoples hospital
Advanced Materials Research | Year: 2013

The tissue samples of cisplatin-resistant and sensitive patients with osteosarcoma were obtained through chemosensitivity testing before. The typical one of cisplatin-resistant and sensitive osteosarcoma tissue samples were analyzed by two-dimensional electrophoresis and the relevant differentially expressed proteins were obtained. The sequences of differentially expressed proteins were obtained through the analysis of mass spectrometry technology to be identified comparing with protein databases. It is concluded that there are differentially expressed proteins in tissue of cisplatin-resistant and sensitive osteosarcoma. © (2013) Trans Tech Publications, Switzerland.

Loading Jilin Province Peoples Hospital collaborators
Loading Jilin Province Peoples Hospital collaborators