Yu Huang Ding Hospital

Yuhuangding, China

Yu Huang Ding Hospital

Yuhuangding, China
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PubMed | Binzhou Medical University and Yu Huang Ding Hospital
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

In order to determine the effect of B7H4 on the development of human hepatocellular carcinoma (HCC), the expression levels of B7H4 were evaluated using reverse transcriptionpolymerase chain reaction and flow cytometry in HL7702 and Huh7 cells. B7H4 protein expression levels were analyzed using western blotting and immunohistochemistry in HCC tissues collected from patients and from a mouse tumor model. Soluble B7H4 (sB7H4), interferon (IFN), and interleukin4 (IL4) in blood serum were assessed using ELISA in patients with HCC and mice injected with tumor cells. B7H4 was expressed in HCC cell lines, mouse tumor tissues and HCC patient tissues. However, B7H4 was not detected in HL7702 cells or normal human liver tissues. The expression level of B7H4 was positively correlated with tumornodemetastasis (TNM) stage, lymph node metastasis, and differentiation degree in patients with HCC. sB7H4 levels in blood serum samples collected from patients with HCC and tumorigenic mice were higher compared with healthy controls. Expression levels of IFN were reduced, and IL4 levels were increased in blood serum samples of patients with HCC and tumorigenic mice compared with healthy controls. sB7H4 expression levels were negatively correlated with IFN levels, and with the ratio of IFN to IL4. Additionally, sB7H4 was positively correlated with IL4 levels in mouse tumor tissues, serum samples obtained from tumorigenic mice and human HCC patients. Notably, the levels of sB7H4 and IL4 were positively correlated and IFN was negatively correlated with the TNM stage of patients with HCC. In addition, sB7H4 and IL4 expression levels increased and levels of IFN and the ratio of IFN/IL4 decreased as a function of time post tumor implantation in the mouse model. The present study determined that aberrant expression of B7H4 contributed to HCC development. B7H4 may be a potential target for therapy and diagnosis of HCC.

PubMed | Linyi Peoples Hospital, Shandong University and Yu Huang Ding Hospital
Type: Journal Article | Journal: PloS one | Year: 2015

Low shear stress (LSS) plays a critical role in the site predilection of atherosclerosis through activation of cellular mechanosensors, such as platelet endothelial cell adhesion molecule 1 (PECAM-1). Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme that regulates the expression of various inflammatory cytokines. The nuclear enzyme high mobility group box 1 (HMGB1) can induce inflammation response by binding to toll-like receptor 4 (TLR4). In the present study, we aimed to investigate the role and mechanism of HMGB1 in LSS induced inflammation in human umbilical vein endothelial cells (HUVECs). HUVECs were stimulated by undisturbed shear stress (USS, 1 Pa) and LSS (0.4 Pa) in our experiments. Gene expression was inhibited by small interfering RNA (siRNA). ICAM-1 expression was regulated by LSS in a time dependent manner. LSS can induce HMGB1 translocation from nucleus to cytoplasm and release. Compared with the USS, LSS could increase the protein expression of PECAM-1 and PARP-1 as well as the secretion of TNF- and IL-1. LSS induced the translocation of HMGB1 from nucleus to cytoplasm. Inhibition of HGMB1 reduced LSS-induced inflammatory response. Inhibition of PARP-1 suppressed inflammatory response through inhibiting TLR4 expression and HMGB1 translocation. PECAM-1 inhibition reduced LSS-induced ICAM-1 expression, TNF- and IL-1 secretion, and monocytes adhesion. LSS can induce inflammatory response via PECAM-1/PARP-1/HMGB1 pathway. PARP-1 plays a fundamental role in HMGB1 translocation and TLR4 expression. Inhibition of PARP-1 may shed light on the treatment of HMGB1 involved inflammation during atherosclerosis.

Guo M.,Yantai Vocational College | Yang A.,Yantai Vocational College | Zhou C.,Bruker Daltonics Inc. | Liu X.,Yu Huang Ding Hospital
Journal of Plant Interactions | Year: 2012

Salt stress is a major abiotic stress limiting the productivity and the geographical distribution of many plant species. Arabidopsis thaliana is an excellent model with rich genetic resources for modern plant biology research. To comprehensively and representatively understand salt-response mechanisms in A. thaliana, we applied the first attempt to use the most data (252 of 10,469 reviewed A. thaliana protein) from public protein database for displaying the enriched protein domains, Kyoto Encyclopedia of Genes and Genomes pathways, molecular functions, and cell localizations involved in salt-response. The data were analyzed by Database for Annotation Visualization and Integrated Discovery. Our results indicated salt-response proteins cross-talked not only with drought and temperature stress as previously reported but also with further stresses such as bacterium, light, metal ion, radiation, and wounding stress. Multiple cellular localizations under salt stress indicated proteins were versatile. In addition, 27 proteins have the characteristics with response to multiple stresses and localization in multiple places. We called it the 'space-stress' double cross-talk effects, which indicated that A. thaliana proteins dealt with salt stress and other stresses in a reciprocal economical way. An enriched bioinformatics analysis of the large data could provide clues and basis for the development of salt-response potential biomarkers for plant growth and crop productivity. © 2012 Copyright Taylor and Francis Group, LLC.

Yu X.,Yu Huang Ding Hospital | Xing C.,Shandong University | Pan Y.,Yu Huang Ding Hospital | Ma H.,Yu Huang Ding Hospital | And 2 more authors.
Acta Biochimica et Biophysica Sinica | Year: 2012

Atherosclerosis, a multifactorial chronic inflammatory response, is closely associated with oxidatively modified low-density lipoprotein (ox-LDL). High-mobility group box 1 (HMGB1) is a DNA-binding protein, which upon release from cells exhibits potent inflammatory action. Insulin-like growth factor 1 (IGF-1) can elicit a repertoire of cellular responses including proliferation and anti-apoptosis. However, the role of IGF-1 in inflammation is still unclear. In the present study, we aimed to investigate the role of IGF-1 in inflammation and the underlying mechanism. Human aortic endothelial cells were stimulated by ox-LDL (50 μg/ml) to induce inflammation. The expression of intercellular adhesion molecule 1 (ICAM-1) was assessed by western blot analysis and immunofluorescence. The release of HMGB1 was determined by enzyme-linked immunosorbent assay. IGF-1 receptor (IGF-1R) expression was assessed by reverse transcription-polymerase chain reaction and western blot analysis. IGF-1R phosphorylation was determined by western blot analysis. Ox-LDL stimulation reduced IGF-1R mRNA and protein expression but increased HMGB1 release. IGF-1 treatment decreased ox-LDL-induced ICAM-1 expression potentially through reducing HMGB1 release, while picropodophyllin, an IGF-1R specific inhibitor, increased the inflammatory response. In conclusion, IGF-1 can alleviate ox-LDL-induced inflammation by reducing HMGB1 release, suggesting an unexpected beneficial role of IGF-1 in inflammatory disease. © 2012 The Author.

Peng X.,Yu Huang Ding Hospital
Acta biochimica et biophysica Sinica | Year: 2012

Atherosclerosis is a chronic inflammatory disease. Toll-like receptor 4 (TLR4) is an important signaling receptor and plays a critical role in the inflammatory response. Poly(ADP-ribose) polymerase 1 (PARP1) is a nuclear enzyme that can regulate the expression of various inflammatory genes. In this study, we investigated the role and the underlying mechanisms of PARP1 on lipopolysaccharide (LPS)-induced inflammation in human aortic endothelial cells. Compared with the control, LPS stimulation increased the protein expression of TLR4 and PARP1. TLR4 inhibition reduced LPS-induced upregulation of inducible nitric oxide synthase (iNOS) and ICAM-1 as well as PARP1. Nuclear factor κB (NF-κB) inhibition decreased ICAM-1 and iNOS expression. Inhibition of PARP1 decreased protein expression of inflammatory cytokines induced by LPS stimulation, probably through preventing NF-κB nuclear translocation. Our study demonstrated that LPS increased ICAM-1 and iNOS expression via TLR4/PARP1/NF-κB pathway. PARP1 might be an indispensable factor in TLR4-mediated inflammation after LPS stimulation. PARP1 inhibition might shed light on the treatment of LPS-induced inflammatory cytokines expression during atherosclerosis.

Liu F.-J.,Yu Huang Ding Hospital | Wang H.-Y.,Yu Huang Ding Hospital | Li J.-Y.,Yu Huang Ding Hospital
Molecular Biology Reports | Year: 2012

The testis is the male gonad responsible for spermatogenesis and steroidogenesis. Much remains to be known about the control of these events. In this study, we performed a new bioinformatic enrichment analysis of human testicular proteins selected from a protein database. Integrated function and pathway analyses were performed by Database for Annotation, Visualization and Integrated Discovery and Ingenuity Pathway Analysis programmes, and significant features were found to be clustered. Proteinmembrane organization and gene density on chromosomes were analyzed and discussed. The analysis could provide a basis for the understanding of testicular physiology and function, and facilitating biological interpretation of testicular functions in a network context. © Springer Science+Business Media B.V. 2011.

Li J.,Yu Huang Ding Hospital | Li J.,Yantai University | Liu F.,Yu Huang Ding Hospital | Wang H.,Yu Huang Ding Hospital | And 9 more authors.
Molecular and Cellular Proteomics | Year: 2010

The mammalian spermatozoon has many cellular compartments, such as head and tail, permitting it to interact with the female reproductive tract and fertilize the egg. It acquires this fertilizing potential during transit through the epididymis, which secretes proteins that coat different sperm domains. Optimal levels of these proteins provide the spermatozoon with its ability to move to, bind to, fuse with, and penetrate the egg; otherwise male infertility results. As few human epididymal proteins have been characterized, this work was performed to generate a database of human epididymal sperm-located proteins involved in maturation. Two-dimensional gel electrophoresis of epididymal tissue and luminal fluid proteins, followed by identification using MALDI-TOF/MS or MALDI-TOF/TOF, revealed over a thousand spots in gels comprising 745 abundant nonstructural proteins, 408 in luminal fluids, of which 207 were present on spermatozoa. Antibodies raised to 619 recombinant or synthetic peptides, used in Western blots, histological sections, and washed sperm preparations to confirm antibody quality and protein expression, indicated their regional location in the epididymal epithelium and highly specific locations on washed functional spermatozoa. Sperm function tests suggested the role of some proteins in motility and protection against oxidative attack. A large database of these proteins, characterized by size, pI, chromosomal location, and function, was given a unified terminology reflecting their sperm domain location. These novel, secreted human epididymal proteins are potential targets for a posttesticular contraceptive acting to provide rapid, reversible, functional sterility in men and they are also biomarkers that could be used in noninvasive assessments of male fertility. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.

Liu F.,Yu Huang Ding Hospital | Wang H.,Yu Huang Ding Hospital | Li J.,Yu Huang Ding Hospital
BMB Reports | Year: 2011

The testis is major male gonad responsible for spermatogenesis and steroidogenesis. Much knowledge is still remained to be learned about the control of these events. In this study, we performed a comprehensive bioinformatics analysis on 1,196 mouse testis proteins screened from public protein database. Integrated function and pathway analysis were performed through Database for Annotation, Visualization and Integrated Discovery (DAVID) and ingenuity Pathway Analysis (IPA), and significant features were clustered. Protein membrane organization and gene density on chromosomes were analyzed and discussed. The enriched bioinformatics analysis could provide clues and basis to the development of diagnostic markers and therapeutic targets for infertility and male contraception.

Wang J.,Shandong University | Wang J.,Yu Huang Ding Hospital | Liu L.,Yu Huang Ding Hospital | Xia Y.,Yu Huang Ding Hospital | Wu D.,Shandong University
Acta Biochimica et Biophysica Sinica | Year: 2014

In addition to biochemical stimuli, physical forces also play a critical role in regulating the structure, function, and metabolism of the lung. Hyperstretch can induce the inflammatory responses in asthma, but the mechanism remains unclear. Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme that can regulate a variety of inflammatory cytokines expression. In the present study, we aimed to investigate the role and mechanism of PARP-1 in mechanical stretch-induced inflammation in human bronchial epithelial cells (HBEpiCs). HBEpiCs were simulated by mechanical stretch and cells under static were used as the control. PARP-1 expression was interfered by small interfering RNA. Oxidative stress was evaluated by DHE staining. DNA damage was assessed by comet assay. The results showed that interleukin-8 (IL-8) and vascular cell adhesion molecule-1 (VCAM-1) expression were regulated by hyperstretch in a time-dependent manner. Hyperstretch could increase PARP-1 expression and activity by inducing superoxide production and DNA damage. Silencing of PARP-1 attenuated hyperstretch-induced IL-8 and VCAM-1 up-regulation as well as monocytes adhesion, which were related to the inhibition of nuclear factor-kappa B (NF-κB) translocation. Our study showed that hyperstretch could induce inflammatory response and superoxide production as well as DNA damage in HBEpiCs. PARP-1 silencing decreased IL-8 and VCAM-1 expression, partly through inhibition of NF-κB translocation. PARP-1 played a fundamental role in hyperstretch-induced inflammation. PARP-1 silencing could be used as a potential therapeutic approach to reverse bronchial epithelial inflammation in asthma. © 2014 The Author 2014.

Dong M.,Shandong University | Zhong L.,Yu Huang Ding Hospital | Chen W.Q.,Shandong University | Ji X.P.,Shandong University | And 8 more authors.
PLoS ONE | Year: 2012

Enhanced matrix metalloproteinases (MMPs) activity is implicated in the process of atherosclerotic plaque instability. We hypothesized that doxycycline, a broad MMPs inhibitor, was as effective as simvastatin in reducing the incidence of plaque disruption. Thirty rabbits underwent aortic balloon injury and were fed a high-fat diet for 20 weeks. At the end of week 8, the rabbits were divided into three groups for 12-week treatment: a doxycycline-treated group that received oral doxycycline at a dose of 10 mg/kg/d, a simvastatin-treated group that received oral simvastatin at a dose of 5 mg/kg/d, and a control group that received no treatment. At the end of week 20, pharmacological triggering was performed to induce plaque rupture. Biochemical, ultrasonographic, pathologic, immunohistochemical and mRNA expression studies were performed. The results showed that oral administration of doxycycline resulted in a significant increase in the thickness of the fibrous cap of the aortic plaque whereas there was a substantial reduction of MMPs expression, local and systemic inflammation, and aortic plaque vulnerability. The incidence of plaque rupture with either treatment (0% for both) was significantly lower than that for controls (56.0%, P<0.05). There was no significant difference between doxycycline-treated group and simvastatin-treated group in any serological, ultrasonographic, pathologic, immunohistochemical and mRNA expression measurement except for the serum lipid levels that were higher with doxycycline than with simvastatin treatment. In conclusion, doxycycline at a common antimicrobial dose stabilizes atherosclerotic lesions via inhibiting matrix metalloproteinases and attenuating inflammation in a rabbit model of vulnerable plaque. These effects were similar to a large dose of simvastatin and independent of serum lipid levels. © 2012 Dong et al.

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