The Experts below are selected from a list of 1239585 Experts worldwide ranked by ideXlab platform
Neil Thomas Young - One of the best experts on this subject based on the ideXlab platform.
-
leukocyte ig like receptor b1 restrains dendritic cell function through Increased Expression of the nf κb regulator abin1 tnip1
Journal of Leukocyte Biology, 2016Co-Authors: Rahul C Khanolkar, Michail Kalogeropoulos, Alistair Lawrie, Ali Roghanian, Mark A Vickers, Neil Thomas YoungAbstract:Inhibitory receptors of the human leukocyte immunoglobulin-like receptor family are constitutively expressed on all myeloid cell types and regulate their functional activity. We demonstrate that ligation of the human leukocyte antigen class I-specific receptor LILRB1, during the differentiation of monocytes to dendritic cells in vitro, results in Increased Expression of the nuclear factor κB inhibitor protein ABIN1 (also known as TNIP1). Similarly Increased Expression of ABIN1/TNIP1 was observed in the "immunosuppressive" monocyte populations of patients with non-Hodgkin lymphoma ex vivo. Reducing Expression of ABIN1/TNIP1 using small interfering ribonucleic acid allows dendritic cells and immunosuppressive monocytes to respond to stimulation by allowing nuclear factor κB translocation to the nucleus (P < 0.001), increasing cell surface Expression of antigen presentation and costimulatory molecules (P < 0.01), increasing phagocytic capacity (P < 0.001), secreting proinflammatory cytokines (P < 0.01), and an increasing ability to stimulate T cell responses (P < 0.05). Our study, therefore, identifies an important functional role for ABIN1/TNIP1 in mediating the effects of LILRB1 ligation-induced inhibitory effects on immune responses. Our findings suggest that inhibiting the LILRB1-ABIN1/TNIP1 pathway in antigen-presenting cells could be a therapeutic approach to stimulate antitumor immune responses. Conversely, stimulation of the pathway may also ameliorate autoimmune diseases in which TNIP1 is a susceptibility gene.
Ali Roghanian - One of the best experts on this subject based on the ideXlab platform.
-
leukocyte ig like receptor b1 restrains dendritic cell function through Increased Expression of the nf κb regulator abin1 tnip1
Journal of Leukocyte Biology, 2016Co-Authors: Rahul C Khanolkar, Michail Kalogeropoulos, Alistair Lawrie, Ali Roghanian, Mark A Vickers, Neil Thomas YoungAbstract:Inhibitory receptors of the human leukocyte immunoglobulin-like receptor family are constitutively expressed on all myeloid cell types and regulate their functional activity. We demonstrate that ligation of the human leukocyte antigen class I-specific receptor LILRB1, during the differentiation of monocytes to dendritic cells in vitro, results in Increased Expression of the nuclear factor κB inhibitor protein ABIN1 (also known as TNIP1). Similarly Increased Expression of ABIN1/TNIP1 was observed in the "immunosuppressive" monocyte populations of patients with non-Hodgkin lymphoma ex vivo. Reducing Expression of ABIN1/TNIP1 using small interfering ribonucleic acid allows dendritic cells and immunosuppressive monocytes to respond to stimulation by allowing nuclear factor κB translocation to the nucleus (P < 0.001), increasing cell surface Expression of antigen presentation and costimulatory molecules (P < 0.01), increasing phagocytic capacity (P < 0.001), secreting proinflammatory cytokines (P < 0.01), and an increasing ability to stimulate T cell responses (P < 0.05). Our study, therefore, identifies an important functional role for ABIN1/TNIP1 in mediating the effects of LILRB1 ligation-induced inhibitory effects on immune responses. Our findings suggest that inhibiting the LILRB1-ABIN1/TNIP1 pathway in antigen-presenting cells could be a therapeutic approach to stimulate antitumor immune responses. Conversely, stimulation of the pathway may also ameliorate autoimmune diseases in which TNIP1 is a susceptibility gene.
Hunter C Champion - One of the best experts on this subject based on the ideXlab platform.
-
Increased Expression of arginase ii in human diabetic corpus cavernosum in diabetic associated erectile dysfunction
International Journal of Impotence Research, 2002Co-Authors: Trinity J Bivalacqua, Wayne J G Hellstrom, Philip J Kadowitz, Hunter C ChampionAbstract:Increased Expression of arginase II in human diabetic corpus cavernosum: in diabetic-associated erectile dysfunction
-
Increased Expression of arginase ii in human diabetic corpus cavernosum in diabetic associated erectile dysfunction
Biochemical and Biophysical Research Communications, 2001Co-Authors: Trinity J Bivalacqua, Wayne J G Hellstrom, Philip J Kadowitz, Hunter C ChampionAbstract:Abstract Nitric oxide (NO) is the principal mediator of penile erection. NO is synthesized by nitric oxide synthase (NOS). It has been well documented that the major causative factor contributing to erectile dysfunction in diabetic patients is the reduction in the amount of NO synthesis in the corpora cavernosa of the penis resulting in alterations of normal penile homeostasis. Arginase is an enzyme that shares a common substrate with NOS, thus arginase may downregulate NO production by competing with NOS for this substrate, l -arginine. The purpose of the present study was to compare arginase gene Expression, protein levels, and enzyme activity in diabetic human cavernosal tissue. When compared to normal human cavernosal tissue, diabetic corpus cavernosum from humans with erectile dysfunction had higher levels of arginase II protein, gene Expression, and enzyme activity. In contrast, gene Expression and protein levels of arginase I were not significantly different in diabetic cavernosal tissue when compared to control tissue. The reduced ability of diabetic tissue to convert l -arginine to l -citrulline via nitric oxide synthase was reversed by the selective inhibition of arginase by 2(S)-amino-6-boronohexanoic acid (ABH). These data suggest that the Increased Expression of arginase II in diabetic cavernosal tissue may contribute to the erectile dysfunction associated with this common disease process and may play a role in other manifestations of diabetic disease in which nitric oxide production is decreased.
Maren U Koban - One of the best experts on this subject based on the ideXlab platform.
-
Increased Expression of extracellular matrix regulators timp1 and mmp1 in deteriorating heart failure
Journal of Heart and Lung Transplantation, 2003Co-Authors: Leanne E Felkin, E J Birks, Paul J R Barton, Martin E Cullen, Maren U KobanAbstract:Abstract Background: The authors previously identified and compared alterations in gene Expression in the myocardia of patients with deteriorating heart failure who underwent left ventricular assist device (LVAD) implantation with those of patients with stable end-stage failure (ESF). We hypothesized that matrix metalloproteinases (MMPs) and their endogenous inhibitors, the tissue inhibitors of MMPs (TIMPs), would be implicated in the mechanisms that underlie deteriorating heart failure. Methods: Gridded macro-array filters were used to provide a broad overview of MMP and TIMP mRNA Expression in heart failure. Precise mRNA levels of TIMP1, MMP1, and β-spectrin were determined using quantitative real-time reverse-transcription polymerase chain reaction (RT-PCR) of myocardial samples from 27 patients with deteriorating heart failure who underwent LVAD implantation, from 17 patients with stable ESF who underwent elective heart transplantation, and from 28 donor organs with good hemodynamic function. Results: Gridded macro-arrays analysis of pooled failing heart samples determined that TIMP1 mRNA was the most readily detectable TIMP in failing myocardium. Quantitative RT-PCR showed that Expression levels in individual patients were similar in patients with stable ESF (1.00 ± 0.24, n = 17) and in donor organ samples (1.49 ± 0.22, n = 28) but were significantly Increased in the deteriorating heart failure group (5.38 ± 0.32, n = 26, p n = 27, p Conclusions: Patients with deteriorating heart failure have Increased Expression of TIMP1 and MMP1 mRNA. Correlation with pro-inflammatory cytokines suggests common pathways of regulation and potential activation by IL-6 and IL1-β.
Peter A Campochiaro - One of the best experts on this subject based on the ideXlab platform.
-
Increased Expression of glutathione peroxidase 4 strongly protects retina from oxidative damage
Antioxidants & Redox Signaling, 2009Co-Authors: Brian C Oveson, Shinichi Usui, Keiichi Komeima, Thomas Lauer, Bing Xie, Peter A CampochiaroAbstract:Abstract Oxidative damage contributes to cone cell death in retinitis pigmentosa and death of rods, cones, and retinal pigmented epithelial (RPE) cells in age-related macular degeneration. In this study, we explored the strategy of overexpressing components of the endogenous antioxidant defense system to combat oxidative damage in RPE cells and retina. In transfected cultured RPE cells with Increased Expression of superoxide dismutase1 (SOD1) or SOD2, there was Increased constitutive and stress-induced oxidative damage measured by the level of carbonyl adducts on proteins. In contrast, RPE cells with Increased Expression of glutathione peroxidase 1 (Gpx1) or Gpx4 did not show an increase in constitutive oxidative damage. An increase in Gpx4, and to a lesser extent Gpx1, reduced oxidative stress-induced RPE cell damage. Co-Expression of Gpx4 with SOD1 or 2 partially reversed the deleterious effects of the SODs. Transgenic mice with inducible Expression of Gpx4 in photoreceptors were generated, and in three...
-
transgenic mice with Increased Expression of vascular endothelial growth factor in the retina a new model of intraretinal and subretinal neovascularization
American Journal of Pathology, 1997Co-Authors: Naoyuki Okamoto, Takao Tobe, Sean F Hackett, H Ozaki, Melissa A Vinores, William J Larochelle, Donald J Zack, Peter A CampochiaroAbstract:Vascular endothelial growth factor (VEGF) has been implicated in retinal neovascularization (NV), but it has been difficult to produce retinal NV with exogenous VEGF. We investigated the effect of Increased VEGF Expression in the retina using tissue-specific, gain-of-function transgenic mice in which the bovine rhodopsin promoter is coupled to the gene for human VEGF. Three founder mice were obtained and used to generate transgenic lines. One of the lines shows Increased Expression of VEGF in the retina by reverse transcription coupled to polymerase chain reaction and Northern blots, and the VEGF is localized to photoreceptors by immunohistochemistry. These mice demonstrate new vessels originating from the deep capillary bed of the retina that extend beneath the photoreceptor layer into the subretinal space where they form clumps of blood vessels surrounded by proliferated retinal pigmented epithelial cells. The appearance is similar to subretinal NV seen in some patients, except that the blood vessels originate from the retinal vasculature rather than the choroidal vasculature. One of the other two lines of mice did not show Increased Expression of VEGF and did not have NV; the other line showed retinal degeneration. This study demonstrates that over-Expression of VEGF in the retina is sufficient to cause intraretinal and subretinal NV and provides a valuable new animal model.
