Attenuation of Experimental Autoimmune Hepatitis in Mice with Bone Mesenchymal Stem Cell-Derived Exosomes Carrying MicroRNA-223-3p

Yong-Ping Chen,Feng-Bin Lu,Da-Zhi Chen,Lu Chen,En-De Hu,Jin-Lu Wu,Hui Li,Yue-Wen Gong,Zhuo Lin,Xiao-Dong Wang,Ji Li,Xiao-Ya Jin,Lan-Man Xu 한국분자세포생물학회 2019 Molecules and cells Vol.42 No.12

MicroRNA-223-3p (miR-223-3p) is one of the potential microRNAs that have been shown to alleviate inflammatory responses in pre-clinical investigations and is highly encased in exosomes derived from bone mesenchymal stem cells (MSC-exosomes). MSC-exosomes are able to function as carriers to deliver microRNAs into cells. Autoimmune hepatitis is one of the challenging liver diseases with no effective treatment other than steroid hormones. Here, we examined whether MSC-exosomes can transfer miR-223-3p to treat autoimmune hepatitis in an experimental model. We found that MSC-exosomes were successfully incorporated with miR-223-3p and delivered miR-223-3p into macrophages. Moreover, there was no toxic effect of exosomes on the macrophages. Furthermore, treatments of either exosomes or exosomes with miR-223-3p successfully attenuated inflammatory responses in the liver of autoimmune hepatitis and inflammatory cytokine release in both the liver and macrophages. The mechanism may be related to the regulation of miR-223-3p level and STAT3 expression in the liver and macrophages. These results suggest that MSC-exosomes can be used to deliver miR-223-3p for the treatment of autoimmune hepatitis.

Biosorption of Chromium (VI) from Electroplating Wastewater using Pine Cone Powder

Chun-Ji Jin,Jiang-Li Shen,Sang-Houck Lee,Bo Xiao,Ping Yang 한국도시환경학회 2010 한국도시환경학회지 Vol.10 No.2

ON TESTING FOR HOMOGENEITY OF THE COVARIANCE N\MATRICES

Zhang, Xiao-Ning,Jing, Ping,Ji, Xiao-Ming 한국전산응용수학회 2001 The Korean journal of computational & applied math Vol.8 No.2

Testing equality of covariance matrix of k populations has long been an interesting issue in statistical inference. To overcome the sparseness of data points in a high-dimensional space and deal with the general cases, we suggest several projection pursuit type statistics. Some results on the limiting distributions of the statistics are obtained. some properties of Bootstrap approximation are investigated. Furthermore, for computational reasons an approximation which is based on Number theoretic method for the statistics is adopted. Several simulation experiments are performed. AMS Subject Classification : 2H15, 62H10, 62G09, 62G10

Novel Anticandidal Activity of a Recombinant Lampetra japonica RGD3 Protein

( Cai Ping Wu ),( Li Lu ),( Yuan Yuan Zheng ),( Xin Liu ),( Rong Xiao ),( Ji Hong Wang ),( Qing Wei Li ) 한국미생물 · 생명공학회 2014 Journal of microbiology and biotechnology Vol.24 No.7

Lj-RGD3, an RGD (Arg-Gly-Asp) toxin protein from the salivary gland of Lampetra japonica,exhibits antifungal activity against Candida albicans. Lj-RGD3 has three RGD motifs and shows homology to histidine-rich glycoprotein. We synthesised two mutant derivatives of Lj-RGD3: Lj-26, which lacks all three RGD motifs and contains no His residues; and Lj-112, which lacks only the three RGD motifs. We investigated the effects of the wild-type and mutated toxins on a gram-positive bacterium (Escherichia coli), a gram-negative bacterium (Staphylococcus aureus), and a fungus (C. albicans). rLj-RGD3 and its mutants exhibited antifungal but not antibacterial activity, as measured by a radial diffusion assay. The C. albicans inhibition zone induced by rLj-112 was larger than that induced by the other proteins, and its inhibitory effect on C. albicans was dose-dependent. In viable-count assays, the rLj-112 MIC was 7.7 μM, whereas the MIC of the positive control (ketoconazole) was 15 μM. Time-kill kinetics demonstrated that rLj-112 effectively killed C. albicans at 1× and 2× MIC within 12 and 6 h, respectively. Electron microscopy analysis showed that rLj-RGD3 and rLj-112 induced C. albicans lysis. Our results demonstrate a novel anticandidal activity for rLj-RGD3 and its mutant derivatives.

Expression of Ang-2/Tie-2 and PI3K/AKT in Colorectal Cancer

Zhang, Ji-Hong,Wang, Li-Hua,Li, Xiang-Jun,Wang, Ai-Ping,Reng, Li-Qun,Xia, Feng-Guo,Yang, Zhi-Ping,Jiang, Jing,Wang, Xiao-Dan,Wen, Chun-Yang Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.20

Purpose: To study the expression of angiogenin-2 (Ang-2) and its receptor Tie-2 in colorectal cancer and discuss the possible mechanisms behind this process. Materials and Methods: Using the streptavidin-peroxidase (SP) immunohistochemical method, paraffin sections from 100 colorectal cancer samples and 10 samples from tumor-adjacent normal tissue (> 2 cm from the edge of the gross tumor) were tested for protein expression of Ang-2, Tie-2, PI3K, and AKT. Reverse transcription-polymerase chain reaction and Western blots were further used to measure expression of the 4 genes and proteins in 20 freshly-resected colorectal cancer samples and tumor-adjacent normal tissues. Results: In colorectal cancer tissues, the expression of the Ang-2, Tie-2, PI3K, and AKT genes and their proteins was significantly higher than in tumor-adjacent normal tissues. Protein expression in poorly-differentiated adenocarcinoma was higher than that in well and moderately differentiated adenocarcinoma. According to Duke's classification, the protein expression in Stages C and D was significantly higher than that in Stages A and B. In the group with lymphatic metastasis, the protein expression was higher than that without lymphatic metastasis. Conclusions: In colorectal cancer, the expression of the Ang-2, Tie-2, PI3K, and AKT genes and their proteins is markedly higher than those in tumor-adjacent normal tissues. No correlation was observed between protein expression and gender, location, or histologic type. Correlations did exist between protein expression and differentiation level, stage of Duke's classification, and lymphatic metastasis; in colorectal cancer tissues with lower differentiation levels, higher stages of Duke's classification, and lymphatic metastasis, the expression of all 4 proteins was higher. The study of their expression patterns and relationships with aggression and metastasis will provide a valuable experimental foundation for assessing prognosis and targeted therapy of colorectal cancer.

Experimental Study of Composite Steel Plate Shear Wall with Flush End-Plate Connection

Jin-Guang Yu,Xiao-Tian Feng,Ji-Ping Hao,Xi Gao 한국강구조학회 2020 International Journal of Steel Structures Vol.20 No.1

This paper presents an investigation on the structural performance of steel plate shear wall (SPSW) with fl ush end-plate beam–column connections and infi ll precast reinforced concrete (precast RC) panels. Two single-span two-story SPSW specimens, including unstiff ened SPSW (NBRP) and precast RC panel restrained SPSW (Con-BRP), are fi rst tested, followed with a parametric study by fi nite element method. Precast RC cover panels are installed on both sides of the infi ll steel plate and are disconnected from steel frame. Test results indicate that the use of precast RC cover panels increases the load carrying and energy dissipation capacities of the SPSW structure, but decreases its ductility. It is also eff ective in reducing the inward fl exural deformation of columns. Moreover, the stiff ening eff ect of the infi ll steel plate on the beam–column connections remains, which is a result of the precast RC cover panel’s resistance to the local buckling and the tears of the infi ll steel plates. The infl uence of the gap size between the precast RC cover plate and frame members on the failure mode of the specimen Con-BRP is also investigated, based on which a maximum gap size is recommended. Conclusions are drawn that SPSW structure with fl ush end-plate beam–column connections and precast RC cover panels fully exploits the strength of infi ll steel plates and exhibits excellent structural performance.

miR-98 suppresses melanoma metastasis through a negative feedback loop with its target gene IL-6

Fei Li,Xin-ji Li,Li Qiao,Fei Shi,Wen Liu,You Li,Yu-ping Dang,Weijie Gu,Xiao-gang Wang,Wei Liu 생화학분자생물학회 2014 Experimental and molecular medicine Vol.46 No.-

Dysregulated microRNA (miRNA) expression has a critical role in tumor development and metastasis. However, the mechanism by which miRNAs control melanoma metastasis is unknown. Here, we report reduced miR-98 expression in melanoma tissues with increasing tumor stage as well as metastasis; its expression is also negatively associated with melanoma patient survival. Furthermore, we demonstrate that miR-98 inhibits melanoma cell migration in vitro as well as metastatic tumor size in vivo. We also found that IL-6 is a target gene of miR-98, and IL-6 represses miR-98 levels via the Stat3-NF-κB-lin28B pathway. In an in vivo melanoma model, we demonstrate that miR-98 reduces melanoma metastasis and increases survival in part by reducing IL-6 levels; it also decreases Stat3 and p65 phosphorylation as well as lin28B mRNA levels. These results suggest that miR-98 inhibits melanoma metastasis in part through a novel miR-98-IL-6-negative feedback loop.

Evaluation on Phytotoxicity of Citrus Peel Extracts to Weeds

Xue-Hua An,Xue-Ping Zhao,Qiang Wang,Xiao-Feng Ji,Chang-Xing Wu 한국잡초학회 2011 한국잡초학회 별책(학술대회 초록집) Vol.31 No.2

An Epigenetic Mechanism Underlying Doxorubicin Induced EMT in the Human BGC-823 Gastric Cancer Cell

Han, Rong-Fei,Ji, Xiang,Dong, Xing-Gao,Xiao, Rui-Jing,Liu, Yan-Ping,Xiong, Jie,Zhang, Qiu-Ping Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.10

The epithelial to mesenchymal transition (EMT) is a key step during embryonic morphogenesis and plays an important role in drug resistance and metastasis in diverse solid tumors. We previously reported that 48 h treatment of anti-cancer drug doxorubicin could induce EMT in human gastric cancer BGC-823 cells. However, the long term effects of this transient drug treatment were unknown. In this study we found that after 48 h treatment with $0.1{\mu}g/ml$ doxorubicin, most cells died during next week, while a minor population of cells survived and formed colonies. We propagated the surviving cells in drug free medium and found that these long term cultured drug survival cells (abbreviated as ltDSCs) retained a mesenchymal-like cell morphology, and expressed high levels of EMT-related molecules such as vimentin, twist and ${\beta}$-catenin. The expression of chromatin reprogramming factors, Oct4 and c-myc, were also higher in ltDSCs than parental cells. We further demonstrated that the protein level of p300 was upregulated in ltDSCs, and inhibition of p300 by siRNA suppressed the expression of vimentin. Moreover, the ltDSCs had higher colony forming ability and were more drug resistant when compared to parental cells. Our results suggested that an epigenetic mechanism is involved in the EMT of ltDSCs.

Darapladib, a Lipoprotein-Associated Phospholipase A2 Inhibitor, Reduces Rho Kinase Activity in Atherosclerosis

Juan Zhang,Dong-Ling Xu,Xiao-Bo Liu,Shao-jie Bi,Tong Zhao,Shu-Jian Sui,Xiao-Ping Ji,Qing-Hua Lu 연세대학교의과대학 2016 Yonsei medical journal Vol.57 No.2

Purpose: Increased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and Rho kinase activity may be associated with atherosclerosis. The principal aim of this study was to examine whether darapladib (a selective Lp-PLA2 inhibitor) could reduce the elevated Lp-PLA2 and Rho kinase activity in atherosclerosis. Materials and Methods: Studies were performed in male Sprague-Dawley rats. The atherosclerosis rats were prepared by feeding them with a high-cholesterol diet for 10 weeks. Low-dose darapladib (25 mg·kg-1·d-1) and high-dose darapladib (50 mg·kg-1·d-1) interventions were then administered over the course of 2 weeks. Results: The serum levels of triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoproteincholesterol (HDL-C), high-sensitivity C-reactive protein (hs-CRP), and Lp-PLA2, significantly increased in atherosclerosis model groups, as did Rho kinase activity and cardiomyocyte apoptosis (p<0.05 vs. sham group), whereas nitric oxide (NO) productionwas reduced. Levels of TC, LDL-C, CRP, Lp-PLA2, and Rho kinase activity were respectively reduced in darapladib groups, whereas NO production was enhanced. When compared to the low-dose darapladib group, the reduction of the levels of TC, LDL-C, CRP, and Lp-PLA2 was more prominent in the high-dose darapladib group (p<0.05), and the increase of NO productionwas more prominent (p<0.05). Cardiomyocyte apoptosis of the high-dose darapladib group was also significantly reduced compared to the low-dose darapladib group (p<0.05). However, there was no significant difference in Rho kinase activity between the low-dose darapladib group and the high-dose darapladib group (p>0.05). Conclusion: Darapladib, a Lp-PLA2 inhibitor, leads to cardiovascular protection that might be mediated by its inhibition of both Rho kinase and Lp-PLA2 in atherosclerosis.