The Experts below are selected from a list of 279 Experts worldwide ranked by ideXlab platform
Elias A Lianos - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of HO-1 mediated attenuation of renal Immune Injury: a gene profiling study.
Translational research : the journal of laboratory and clinical medicine, 2011Co-Authors: Pu Duann, Elias A LianosAbstract:Using a mouse model of Immune Injury directed against the renal glomerular vasculature and resembling human forms of glomerulonephritis (GN), we assessed the effect of targeted expression of the cytoprotective enzyme heme oxygenase (HO)-1. A human (h) HO-1 complementary DNAN (cDNA) sequence was targeted to glomerular epithelial cells (GECs) using a GEC-specific murine nephrin promoter. Injury by administration of antibody against the glomerular basement membrane (anti-GBM) to transgenic (TG) mice with GEC-targeted hHO-1 was attenuated compared with wild-type (WT) controls. To explore changes in the expression of genes that could mediate this salutary effect, we performed gene expression profiling using a microarray analysis of RNA isolated from the renal cortex of WT or TG mice with or without anti-GBM antibody-induced Injury. Significant increases in expression were detected in 9 major histocompatibility complex (MHC)-class II genes, 2 interferon-γ (IFN-γ)–inducible guanosine triphosphate (GTP)ases, and 3 genes of the ubiquitin-proteasome system. The increase in MHC-class II and proteasome gene expression in TG mice with Injury was validated by real-time polymerase chain reaction (PCR) or Western blot analysis. The observations point to novel mechanisms underlying the cytoprotective effect of HO-1 in renal Immune Injury.
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superoxide dismutase mimetic preserves the glomerular capillary permeability barrier to protein
Journal of Pharmacology and Experimental Therapeutics, 2006Co-Authors: Pu Duann, Prasun K Datta, Jeffrey B Blumberg, Mukut Sharma, Elias A LianosAbstract:Overproduction of superoxide (![Formula][1] ) occurs in glomerular disease and may overwhelm the capacity of superoxide dismutase (SOD), thereby intensifying oxidant Injury by ![Formula][2] and related radical species that disrupt the glomerular capillary permeability barrier to protein. We examined the efficacy of the SOD mimetic tempol in preserving glomerular permeability to protein using 1) a rat model of glomerular Immune Injury induced by an antiglomerular basement membrane antibody (anti-GBM), and 2) isolated rat glomeruli in which Injury was induced by the cytokine tumor necrosis factor-α (TNFα). To induce glomerular Immune Injury, rats received anti-GBM using a protocol that results in prominent infiltration of glomeruli by macrophages and in which macrophage-derived TNFα has been shown to mediate albuminuria. To increase glomerular capillary permeability to albumin (Palb) ex vivo, isolated glomeruli were incubated with TNFα at concentrations (0.5–4.0 μg/ml) known to stimulate ![Formula][3] production. Increments in Palb were detected by measuring changes in glomerular volume in response to an applied oncotic gradient. Significant increases in the urine excretion of albumin and F2α-isoprostane were observed in rats with glomerular Immune Injury without a significant change in systolic blood pressure. Tempol treatment significantly reduced urine isoprostane and albumin excretion. In isolated glomeruli, TNFα increased Palb and tempol abrogated this effect, both in a dose-dependent manner. These observations indicate that SOD mimetics can preserve the glomerular permeability barrier to protein under conditions of oxidative stress from ![Formula][4] production. [1]: /embed/tex-math-1.gif [2]: /embed/tex-math-2.gif [3]: /embed/tex-math-3.gif [4]: /embed/tex-math-4.gif
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Effect of nitric oxide synthase inhibition on proteinuria in glomerular Immune Injury.
Experimental biology and medicine (Maywood N.J.), 2006Co-Authors: Prasun K Datta, Pu Duann, Mukut Sharma, Elias A LianosAbstract:In glomerular Immune Injury, the inducible isoform of nitric oxide synthase (iNOS) becomes a major catalyst of NO production. Although iNOS-catalyzed NO production is sustained and can be cytotoxic, iNOS inhibition exacerbates the magnitude of proteinuria that accompanies Immune Injury. To investigate putative mechanisms of this effect, we assessed changes in glomerular permeability to albumin by using the following two approaches: (i) an in vivo rat model of glomerular Immune Injury induced by antibody against the glomerular basement membrane (GBM), in which urine albumin excretion was measured under conditions of iNOS inhibition, and (ii) an ex vivo model of isolated rat glomeruli, in which changes in glomerular capillary permeability to albumin were assessed under conditions of NOS inhibition. In rats with anti-GBM antibody-induced glomerular Injury, there was an increase in urine albumin excretion. Treatment with two structurally dissimilar iNOS inhibitors at doses sufficient to decrease urine nitrate and/or nitrite exacerbated proteinuria. In these animals, urine excretion of the isoprostane 8-iso-PGF2alpha (marker of oxidative stress) was increased. In isolated glomeruli incubated with the NOS inhibitor L-NMMA, the permeability to albumin increased. This effect was reversed by the NO donor DETA NONOate and by the superoxide dismutase mimetic Tempol. We conclude that NOS-catalyzed NO production is an important mechanism in regulating glomerular permeability to protein. This mechanism involves control of the bioavailability of superoxide.
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Long-term effect of heme oxygenase (HO)-1 induction in glomerular Immune Injury.
The Journal of laboratory and clinical medicine, 2006Co-Authors: Prasun K Datta, Pu Duann, Elias A LianosAbstract:In a rat model of macrophage-dependent glomerular Immune Injury induced by administration of antibody against the glomerular basement membrane (anti-GBM), the authors assessed the anti-proteinuric effect of Heme Oxygenase-1 (HO-1) induction. Rats received anti-GBM antibody alone, anti-GBM antibody and treatment with the HO-1 inducer, hemin, or non-Immune serum (controls). Urine protein, creatinine, and nitrite/nitrate excretion were measured on days 5, 7, and 14 after administration of the anti-GBM antibody. In hemin-treated animals with anti-GBM antibody-induced Immune Injury, HO-1 immunolocalized in macrophages infiltrating glomeruli and in tubular epithelial cells. In these animals, proteinuria was decreased. There was also a decrease in blood urea nitrogen (BUN) levels without a change in serum creatinine or systemic blood pressure. The observations establish the anti-proteinuric effect of hemin induction. This effect could be mechanistically linked to blunting of the ability of infiltrating macrophages to cause Injury or to changes in tubular handling of filtered protein.
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Enhanced expression of the cytoskeleton-associated proteins paxillin and focal adhesion kinase in glomerular Immune Injury.
The Journal of laboratory and clinical medicine, 1999Co-Authors: Sevasti B. Koukouritaki, Ashraf Tamizuddin, Elias A LianosAbstract:Abstract In a rat model of glomerular Immune Injury induced by antibody against the glomerular basement membrane (GBM), we assessed changes in the levels and in the extent of tyrosine phosphorylation of two cytoskeleton-associated proteins, focal adhesion kinase (FAK) and paxillin. Glomeruli were isolated 2, 7, and 14 days after the administration of a rabbit anti-rat GBM antibody that induced proliferative nephritis and proteinuria. FAK and paxillin levels in glomerular protein lysates were assessed by immunoprecipitation followed by Western blot analysis. Changes in the tyrosine phosphorylation of immunoprecipitated paxillin and FAK were assessed by Western blot analysis with antiphosphotyrosine antibodies. Glomerular levels of FAK and paxillin were increased in nephritic glomeruli as compared with non-nephritic controls at all time points. There was a discordant increase in the tyrosine phosphorylation levels of paxillin and FAK; the increase in the tyrosine phosphorylation of FAK was sustained and peaked on day 7 of Immune Injury, whereas that of paxillin was short-lived and peaked on day 2 of Injury. We propose that these changes in FAK and paxillin expression and tyrosine phosphorylation reflect interactions between glomerular cells and accumulating extracellular matrix proteins in the course of Immune Injury, or they constitute parts of wider signaling events within the nephritic glomerulus that involve the cytoskeleton. (J Lab Clin Med 1999;134:173-79)
Bo Dong - One of the best experts on this subject based on the ideXlab platform.
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Bcl-xL overexpression restricts γ-radiation-induced apoptosis
Cell Biology International, 2005Co-Authors: Zi-bing Wang, Ying Zhang, Han Xu, Bo DongAbstract:Bcl-xL belongs to a family of proteins which inhibit apoptosis in a number of stimuli including ionizing radiation. To better understand the effects and mechanisms of Bcl-xL on the apoptosis of lymphocytes and provide experimental basis to treat Immune Injury induced by radiation, we used normal human lymphoblastoid AHH-1 cells that were engineered to overexpress Bcl-xL proteins. Our results showed that overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1-Bcl-xL cells were also lower compared to parental AHH-1 cells. Unexpectedly, the fluorescence intensity of Rhodomine 123 (Rh 123) for measuring mitochondrial membrane potential (MMP) did not change at all detected time points. These results possess a vital significance for insights into a new strategy for gene therapy of radiation-induced Immune Injury.
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Bcl‐xL overexpression restricts γ‐radiation‐induced apoptosis
Cell biology international, 2005Co-Authors: Zi-bing Wang, Ying Zhang, Bo Dong, Yu-qing Liu, Ying Guo, Yu-fang CuiAbstract:Bcl-xL belongs to a family of proteins which inhibit apoptosis in a number of stimuli including ionizing radiation. To better understand the effects and mechanisms of Bcl-xL on the apoptosis of lymphocytes and provide experimental basis to treat Immune Injury induced by radiation, we used normal human lymphoblastoid AHH-1 cells that were engineered to overexpress Bcl-xL proteins. Our results showed that overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1-Bcl-xL cells were also lower compared to parental AHH-1 cells. Unexpectedly, the fluorescence intensity of Rhodomine 123 (Rh 123) for measuring mitochondrial membrane potential (MMP) did not change at all detected time points. These results possess a vital significance for insights into a new strategy for gene therapy of radiation-induced Immune Injury.
Zi-bing Wang - One of the best experts on this subject based on the ideXlab platform.
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Bcl-xL overexpression restricts γ-radiation-induced apoptosis
Cell Biology International, 2005Co-Authors: Zi-bing Wang, Ying Zhang, Han Xu, Bo DongAbstract:Bcl-xL belongs to a family of proteins which inhibit apoptosis in a number of stimuli including ionizing radiation. To better understand the effects and mechanisms of Bcl-xL on the apoptosis of lymphocytes and provide experimental basis to treat Immune Injury induced by radiation, we used normal human lymphoblastoid AHH-1 cells that were engineered to overexpress Bcl-xL proteins. Our results showed that overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1-Bcl-xL cells were also lower compared to parental AHH-1 cells. Unexpectedly, the fluorescence intensity of Rhodomine 123 (Rh 123) for measuring mitochondrial membrane potential (MMP) did not change at all detected time points. These results possess a vital significance for insights into a new strategy for gene therapy of radiation-induced Immune Injury.
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Bcl‐xL overexpression restricts γ‐radiation‐induced apoptosis
Cell biology international, 2005Co-Authors: Zi-bing Wang, Ying Zhang, Bo Dong, Yu-qing Liu, Ying Guo, Yu-fang CuiAbstract:Bcl-xL belongs to a family of proteins which inhibit apoptosis in a number of stimuli including ionizing radiation. To better understand the effects and mechanisms of Bcl-xL on the apoptosis of lymphocytes and provide experimental basis to treat Immune Injury induced by radiation, we used normal human lymphoblastoid AHH-1 cells that were engineered to overexpress Bcl-xL proteins. Our results showed that overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1-Bcl-xL cells were also lower compared to parental AHH-1 cells. Unexpectedly, the fluorescence intensity of Rhodomine 123 (Rh 123) for measuring mitochondrial membrane potential (MMP) did not change at all detected time points. These results possess a vital significance for insights into a new strategy for gene therapy of radiation-induced Immune Injury.
Jiaxiang Zhang - One of the best experts on this subject based on the ideXlab platform.
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endothelin 1 endothelin receptor type a angiopoietins tie 2 pathway in regulating the cross talk between glomerular endothelial cells and podocytes in trichloroethylene induced renal Immune Injury
Journal of Inflammation Research, 2021Co-Authors: Haibo Xie, Hui Wang, Jiale Peng, Hua Huang, Yican Wang, Meng Huang, Wei Jiang, Yi Yang, Xuesong Zhang, Jiaxiang ZhangAbstract:Introduction This study aimed to investigate the mechanism in regulating the cross talk between glomerular endothelial cells and podocytes in "occupational medicamentosa-like dermatitis induced by trichloroethylene (OMLDT)" patients. Methods Totally 6 OMLDT patients, 18 controls, and 102 BALB/c female mice were involved in this study. Patient's serum endothelin-1 (ET-1), angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2), blood urea nitrogen (BUN), and podocalyxin (PCX) were detected. All the mice were used to establish the trichloroethylene (TCE) sensitized mouse model. Transmission electron microscope results were used to reflect renal glomerulus Injury. Protein levels were detected by Western blot. Ang-1/Ang-2 gene level was reflected by RT-PCR. Cell apoptosis level was detected by using TUNEL assay kit. Results We found that in OMLDT patients, ET-1, Ang-2, BUN, and PCX were highly expressed but Ang-1 was inhibited. In TCE sensitized positive mouse, the downregulation of Ang-1, pTie-2 and the upregulation of Ang-2 were mediated by ET-1/ETAR but not ET-1/ETBR. The promotor of apoptosis proteins was downregulated and the inhibitor of apoptosis proteins was upregulated by treating with BQ123. Discussion ET-1/ETAR-Angs/Tie-2 pathway mediated the cross talk between glomerular endothelial cells and podocytes. BQ123 can alleviate glomerulus Immune Injury.
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Role of complement regulatory protein CD55 in the liver Immune Injury of trichloroethylene-sensitized mice
Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational di, 2017Co-Authors: Xian Wang, Peng Yang, X D Yang, Jiaxiang Zhang, C Zhang, Qixing ZhuAbstract:Objective: To explore the expression of CD55 in liver tissue of trichloroethylene-sensitized mice and discuss the role of CD55 in the liver Immune Injury of trichloroethylene-sensitized mice. Methods: 6-8 weeks specific pathogen free female BALB/c were randomly divided into blank control group, solvent control group and TCE treatment group to establish BALB/c mice sensitized model. According to mouse skin sensitization reaction score, TCE treatment mice were divided into sensitized and non-sensitized group at 24 h after the last challenge. At 48 h after the last challenge, the blood and aseptic livers were collected. The level of serum ALT was tested by automatic biochemical analyzer and pathology of the liver was observed. C5b-9 deposition was studied by immunohistochemistry (IHC) . CD55 protein expression level in liver tissue was studied by immunohistochemistry and Western blotting. The expression of CD55 mRNA in liver tissue was detected by qRT-PCR. Results: Liver function test result showed level of serum ALT in TCE sensitized group was significantly higher than solvent control group and TCE non-sensitized group (P
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the effect of complement c3a receptor antagonist in the kidney Immune Injury in trichloroethylene sensitized mice
Chinese Journal of Industrial Hygiene and Occupational Diseases, 2017Co-Authors: Peng Yang, D D Zang, X D Yang, Xian Wang, Jiaxiang Zhang, Qixing ZhuAbstract:Objective To explore the effect of complement C3 a-C3a receptor in the kidney Immune inju-ry in trichloroethylene-sensitized mice by using C3a receptor specific antagonist C3aRA and discuss the patho-genesis of kidney Injury in occupational dermatitis medicamentosa-like of trichloroethylene (ODMLT) . Methods 42 female 6~8 weeks old BALB/c mice of specific pathogen free were randomly divided into blank control group (5) , solvent control group (5) , TCE treatment group (16) and TCE+C3aRA treatment group (16) . The TCE treat-ment group and TCE+C3aRA treatment group were further divided into the sensitized group and the non-sensi-tized group according to the skin sensitization test score. Renal function was detected by biochemical detection kit; expression of C3aR in kidney tissue was detected by qPCR; expression of IL-1β and TNF-α protein were de-tected by immunohistochemical. Results Compared with solvent control group and corresponding non-sensitized group, CRE and BUN in TCE sensitized group and TCE + C3aRA sensitized group were significantly increased (P<0.05) . Compared with TCE sensitized group, CRE and BUN in TCE+C3aRA sensitized group were signifi-cantly decreased (P<0.05) . Compared with solvent control group and TCE non-sensitized group, the expression level of C3aR gene in kidney tissue in TCE sensitized group was significantly increased (P<0.05) . There was a large number of IL-1β and TNF-α protein expression in kidney tissue in TCE sensitized group and TCE+C3aRA sensitized group. Compared with the TCE sensitized group, the expression level of IL-1β and TNF-α protein in kidney tissue in TCE+C3aRA sensitized group was significantly decreased (P<0.05) . Conclusion C3a-C3aR may be involved in the kidney Immune Injury in TCE sensitized mice, C3aRA has a protective effect on the kid-ney Immune Injury in TCE sensitized mice. Key words: Trichloroethylene; Kidney; C3aR; Interleukins; Tumor necrosis factor
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Study on the expression of bradykinin and its receptors B1R and B2R in the kidney Immune Injury in trichloroethylene-sensitized mouse
Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational di, 2015Co-Authors: Hui Wang, Jiaxiang Zhang, Wan-sheng Zha, Feng Wang, Qixing ZhuAbstract:Objective To study the expression of bradykinin and its receptors B1R and B2R in the kidney Immune Injury in trichloroethylene-sensitized mouse and discuss the pathogenesis of Dermatitis Medicamentosalike of TCE (ODMLT). Methods On the first days, intradermal injection by 50% TCE and the amount of FCA mixture 100μl for initial sensitization; on 4, 7, 10 days, painted abdominal skin by 100 μl 50% TCE for three sensitization, on 17, 19 days, painted on the back skin by 100 μl 30% TCE for initial excitation and the last challenge; 24 h before each challenge, PKSI-527+TCE group received intraperitoneal injection by inhibitor PKSI-527 (50 mg/kg); solvent control group treat without TCE and sensitization and excitation reagent the same proportion of olive oil and acetone mixture, blank control group without any treatment. Before killing the mouse, renal weight and body weight were recorded. The renals and plasma were separated at 24 h, 48 h, 72 h and 7 d after the last challenge and observed pathological of the renals. Expression of B1R and B2R in renal were examined by immunofluorescence technique. Plasma were examined by ELISA for BK. Results The renal pathological examination revealed the apparent damage of TCE sensitized mice which compared to solvent control group showed obvious cellular infiltration, vacuolar degeneration of renal tubular epithelial cells. The renal damage of PKSI-527+TCE-sensitized groups which compared to the corresponding point of TCE-sensitized groups showed significantly reduced. The expression of BK in 24 h, 48 h and 72 h TCE-sensitized groups were significant higher than solvent control group and related TCE non-sensitized groups (P
Yu-fang Cui - One of the best experts on this subject based on the ideXlab platform.
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Bcl‐xL overexpression restricts γ‐radiation‐induced apoptosis
Cell biology international, 2005Co-Authors: Zi-bing Wang, Ying Zhang, Bo Dong, Yu-qing Liu, Ying Guo, Yu-fang CuiAbstract:Bcl-xL belongs to a family of proteins which inhibit apoptosis in a number of stimuli including ionizing radiation. To better understand the effects and mechanisms of Bcl-xL on the apoptosis of lymphocytes and provide experimental basis to treat Immune Injury induced by radiation, we used normal human lymphoblastoid AHH-1 cells that were engineered to overexpress Bcl-xL proteins. Our results showed that overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1-Bcl-xL cells were also lower compared to parental AHH-1 cells. Unexpectedly, the fluorescence intensity of Rhodomine 123 (Rh 123) for measuring mitochondrial membrane potential (MMP) did not change at all detected time points. These results possess a vital significance for insights into a new strategy for gene therapy of radiation-induced Immune Injury.
