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Xiaoqiu Zhou - One of the best experts on this subject based on the ideXlab platform.
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gill structural integrity changes in fish deficient or excessive in dietary isoleucine towards the modulation of Tight Junction Protein inflammation apoptosis and antioxidant defense via nf κb tor and nrf2 signaling pathways
Fish & Shellfish Immunology, 2017Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu Zhou, Wuneng TangAbstract:This study firstly aimed to test the impact of dietary isoleucine (Ile) on Tight Junction Protein, inflammation, apoptosis, antioxidant defense and related signaling molecule gene expression in the gill of fish. Young grass carp (Ctenopharyngodon idella) (weighing 256.8 ± 3.5 g) were fed six diets containing graded levels of Ile, namely, 3.8, 6.6, 9.3, 12.5, 15.2 and 18.5 g/kg diet for 8 weeks. The results firstly revealed that Ile deficiency down-regulated the mRNA expressions of claudin-3, claudin-b, claudin-c, occludin and zonula occludens-1 (ZO-1) and up-regulated the mRNA expression of claudin-12, which led to the intercellular structure damage of fish gill. These effects were partially ascribed to the up-regulation of pro-inflammatory cytokines [interleukin 1β (IL-1β), interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α)] mRNA expressions that referring to up-regulated nuclear factor κB P65 (NF-κB P65) mRNA expression and down-regulated inhibitor factor κBα (IκBα) mRNA expression, and the down-regulation of anti-inflammatory cytokines [interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1)] mRNA expressions that referring to the down-regulated TOR and S6K1 mRNA expression. Interestingly, no change in claudin 15 mRNA level was observed among every treatment. At the same time, the results firstly indicated that Ile deficiency also resulted in the cellular structure damage of fish gill: (1) DNA fragmentation partially due to the up-regulation of caspase-3, caspase-8 and caspase-9 mRNA expression; (2) increase in Protein carbonyl (PC), malondialdehyde (MDA) and ROS contents, which may be partially attributed to the impaired antioxidant defense [indicated by decreased glutathione (GSH) level and depressed anti-superoxide anion (ASA), anti-hydroxyl radical (a-HR), copper/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT) and glutathione peroxidase (GPx) activities] that referring to the down-regulation of corresponding antioxidant enzyme mRNA expressions and the related signaling molecules Nrf2 mRNA expression. Ile excess caused similar negative effects that observed in Ile-deficient group, whereas these negative effects were reversed with appropriate Ile supplementation. In conclusion, our results indicated that Ile deficiency or excess disrupted the structural integrity of fish gill, partially due to the trigger of apoptosis, the impairment of antioxidant defense, and the regulation of Tight Junction Protein, inflammatory cytokines, apoptosis-related, antioxidant enzymes and related signaling molecules mRNA expressions in the fish gill.
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changes in barrier health status of the gill for grass carp ctenopharyngodon idella during valine deficiency regulation of Tight Junction Protein transcript antioxidant status and apoptosis related gene expression
Fish & Shellfish Immunology, 2015Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu ZhouAbstract:This study investigated the effects of dietary valine on Tight Junction Protein transcription, antioxidant status and apoptosis on grass carp gills (Ctenopharyngodon idella). Fish were fed six different experimental diets containing graded levels of valine (4.3, 8.0, 10.6, 13.1, 16.7, 19.1 g/kg). The results indicated that valine deficiency decreased Claudin b, Claudin 3, Occludin and ZO-1 transcription and increased Claudin 15 expression in the fish gill (P 0.05). Valine deficiency also disrupted antioxidant status in the gill by decreasing anti-superoxide radicals and hydroxyl radical capacity, glutathione contents and the activities and mRNA levels of Cu/Zn superoxide dismutase (SOD1), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) (P < 0.05). These results may be ascribed to the down-regulation of NF-E2-related factor 2 (Nrf2), target of rapamycin (TOR) and ribosomal Protein S6 kinase 1 (S6K1) and the up-regulation of Kelch-like-ECH-associated Protein 1 (Keap1) (P < 0.05). Additionally, valine deficiency induced DNA fragmentation via the up-regulation of Caspase 3, Caspase 8 and Caspase 9 expressions (P < 0.05). These results may be ascribed to the improvement in ROS levels in the fish gill (P < 0.05). Taken together, the results showed that valine deficiency impaired the structural integrity of fish gill by disrupted fish antioxidant defenses and regulating the expression of Tight Junction Protein, cytokines, antioxidant enzymes, NF-kappa B p65, I kappa B alpha, TOR, Nrf2, Keap1 and apoptosis-related genes in the fish gill. (C) 2015 Elsevier Ltd. All rights reserved.
Walter A Koltun - One of the best experts on this subject based on the ideXlab platform.
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increase in the Tight Junction Protein claudin 1 in intestinal inflammation
Digestive Diseases and Sciences, 2011Co-Authors: Lisa S Poritz, Leonard R Harris, Ashley A Kelly, Walter A KoltunAbstract:Background and Aims Studies have shown a decrease in key Tight Junction (TJ) Proteins such as ZO-1 and occludin in both inflammatory bowel disease (IBD) and experimental models of inflammation. Our group has also shown an increase in claudin-1 in experimental colitis.
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loss of the Tight Junction Protein zo 1 in dextran sulfate sodium induced colitis
Journal of Surgical Research, 2007Co-Authors: Lisa S Poritz, Kristian I Garver, Cecelia L Green, Leo R Fitzpatrick, Francesca Ruggiero, Walter A KoltunAbstract:Background Inflammatory bowel disease (IBD) is associated with increased intestinal permeability and decreased expression of Tight Junction (TJ) Proteins in the inflamed mucosa. Whether this alteration in TJ expression is a prerequisite for the development of intestinal inflammation or a secondary result of that inflammation is unknown. This study looked at the expression of the TJ Protein ZO-1 and the corresponding permeability changes in dextran sulfate sodium (DSS) induced colitis in a mouse model. Materials and methods BALB/c mice were fed 3% DSS or water for 1, 3, 5, or 7 days. The animals were weighed, stool was checked for blood, and the colon length measured. Segments of the colon were used for histology, immunohistochemistry for ZO-1, or Western blot for TJ Proteins. Colonic permeability was measured using Evan's Blue dye. Results DSS treated animals had heme positive stools, colitis by histology, significant weight loss, and colon shortening. There was an absence of ZO-1 by Western blot in the 7-day DSS treated animals, double the amount of claudin-1 and normal cytokeratin. The loss of ZO-1 started after 1 d of DSS treatment and was followed by a significant increase in permeability to Evan's blue by day 3. Conclusions The loss of ZO-1 and increased permeability preceded the development of significant intestinal inflammation suggesting that in DSS colitis alterations in the TJ complex occur before the intestinal inflammation and not as a consequence of it. These changes in the TJ complex may facilitate the development of the inflammatory infiltrate seen in colitis.
Matthias Bruewer - One of the best experts on this subject based on the ideXlab platform.
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probiotic mixture vsl 3 protects the epithelial barrier by maintaining Tight Junction Protein expression and preventing apoptosis in a murine model of colitis
American Journal of Physiology-gastrointestinal and Liver Physiology, 2009Co-Authors: Rudolf Mennigen, Kerstin Nolte, E Rijcken, Markus Utech, Bettina Loeffler, Norbert Senninger, Matthias BruewerAbstract:Changes in epithelial Tight Junction Protein expression and apoptosis increase epithelial permeability in inflammatory bowel diseases. The effect of the probiotic mixture VSL#3 on the epithelial ba...
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Probiotic mixture VSL#3 protects the epithelial barrier by maintaining Tight Junction Protein expression and preventing apoptosis in a murine model of colitis.
American Journal of Physiology-gastrointestinal and Liver Physiology, 2009Co-Authors: Rudolf Mennigen, Kerstin Nolte, E Rijcken, Markus Utech, Bettina Loeffler, Norbert Senninger, Matthias BruewerAbstract:Changes in epithelial Tight Junction Protein expression and apoptosis increase epithelial permeability in inflammatory bowel diseases. The effect of the probiotic mixture VSL#3 on the epithelial ba...
Weidan Jiang - One of the best experts on this subject based on the ideXlab platform.
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gill structural integrity changes in fish deficient or excessive in dietary isoleucine towards the modulation of Tight Junction Protein inflammation apoptosis and antioxidant defense via nf κb tor and nrf2 signaling pathways
Fish & Shellfish Immunology, 2017Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu Zhou, Wuneng TangAbstract:This study firstly aimed to test the impact of dietary isoleucine (Ile) on Tight Junction Protein, inflammation, apoptosis, antioxidant defense and related signaling molecule gene expression in the gill of fish. Young grass carp (Ctenopharyngodon idella) (weighing 256.8 ± 3.5 g) were fed six diets containing graded levels of Ile, namely, 3.8, 6.6, 9.3, 12.5, 15.2 and 18.5 g/kg diet for 8 weeks. The results firstly revealed that Ile deficiency down-regulated the mRNA expressions of claudin-3, claudin-b, claudin-c, occludin and zonula occludens-1 (ZO-1) and up-regulated the mRNA expression of claudin-12, which led to the intercellular structure damage of fish gill. These effects were partially ascribed to the up-regulation of pro-inflammatory cytokines [interleukin 1β (IL-1β), interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α)] mRNA expressions that referring to up-regulated nuclear factor κB P65 (NF-κB P65) mRNA expression and down-regulated inhibitor factor κBα (IκBα) mRNA expression, and the down-regulation of anti-inflammatory cytokines [interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1)] mRNA expressions that referring to the down-regulated TOR and S6K1 mRNA expression. Interestingly, no change in claudin 15 mRNA level was observed among every treatment. At the same time, the results firstly indicated that Ile deficiency also resulted in the cellular structure damage of fish gill: (1) DNA fragmentation partially due to the up-regulation of caspase-3, caspase-8 and caspase-9 mRNA expression; (2) increase in Protein carbonyl (PC), malondialdehyde (MDA) and ROS contents, which may be partially attributed to the impaired antioxidant defense [indicated by decreased glutathione (GSH) level and depressed anti-superoxide anion (ASA), anti-hydroxyl radical (a-HR), copper/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT) and glutathione peroxidase (GPx) activities] that referring to the down-regulation of corresponding antioxidant enzyme mRNA expressions and the related signaling molecules Nrf2 mRNA expression. Ile excess caused similar negative effects that observed in Ile-deficient group, whereas these negative effects were reversed with appropriate Ile supplementation. In conclusion, our results indicated that Ile deficiency or excess disrupted the structural integrity of fish gill, partially due to the trigger of apoptosis, the impairment of antioxidant defense, and the regulation of Tight Junction Protein, inflammatory cytokines, apoptosis-related, antioxidant enzymes and related signaling molecules mRNA expressions in the fish gill.
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the Tight Junction Protein transcript abundance changes and oxidative damage by tryptophan deficiency or excess are related to the modulation of the signalling molecules nf κb p65 tor caspase 3 8 9 and nrf2 mrna levels in the gill of young grass carp
Fish & Shellfish Immunology, 2015Co-Authors: Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Wuneng Tang, Juan Zhao, Yongan ZhangAbstract:This study is for the first time to explore the possible effects of dietary tryptophan (Trp) on structural integrity and the related signalling factor gene expression in the gill of young grass carp (Ctenopharyngodon idella). Fish were fed with six different experimental diets containing graded levels of Trp at 0.7 (control), 1.7, 3.1, 4.0, 5.2 and 6.1 g kg(-1) diet for 8 weeks. The results firstly demonstrated that Trp deficiency or excess caused increases in reactive oxygen species (ROS) contents, and severe oxidative damage (lipid peroxidation and Protein oxidation) in the gill of fish, and those negative effects could be reversed by optimal Trp levels. Secondly, compared with the optimal Trp levels, Trp deficiency could cause decreases in the mRNA levels of the barrier functional Proteins (occludin, zonula occludens-1, claudin-c, and -3) and increases in the mRNA levels of the pore-formation Proteins (claudin-12 and -15) mRNA levels in the gill of fish, and those were reversed by the optimal levels of Trp. The negative effects of Trp deficiency on those Tight Junction Protein gene expression might be partly related to the increases in the mRNA levels of pro-inflammatory cytokines and related signalling factors (tumor necrosis factor a, interleukin 8, interleukin 10 and transcription factor-kappa B) and decreases in the mRNA levels of anti-inflammatory cytokines and related signalling factors [interleukin 10, transforming growth factor-beta 1, nuclear inhibitor factor kappa B alpha (i kappa B alpha), target of rapamyc and ribosome Protein S6 kinase 1 (S6K1)] in the gill of fish. In addition, optimal dietary Trp protected the gill of fish against its deficiency-caused increases in the mRNA levels of the apoptosis signalling (caspase-3, caspase-8, caspase-9) and decreases in anti-superoxide radicals capacity, anti-hydroxyl radical capacity, glutathione contents and the activities of Cu/Zn superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) in the gill of fish. Additionally, compared with the Trp deficiency, optimal Trp up-regulated the mRNA levels of SOD, CAT, GPx, GR and GST, which might be partly ascribed to the up-regulation of the NF-E2-related factor 2 (Nrf2) mRNA levels and the down-regulation of Kelch-like-ECH-associated Protein 1 (Keap1) mRNA levels in the gill of fish. Interestingly, excessive Trp caused similar results with its deficiency. Collectively, Trp deficiency or excess could cause antioxidant system disruption and change Tight Junction Protein transcription abundances, which were partly related to the signalling factors, NF-kappa B p65, TOR, caspase-(3,8,9) and Nrf2, in fish gill, those could be blocked by the optimal Trp levels. (C) 2015 Elsevier Ltd. All rights reserved.
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changes in barrier health status of the gill for grass carp ctenopharyngodon idella during valine deficiency regulation of Tight Junction Protein transcript antioxidant status and apoptosis related gene expression
Fish & Shellfish Immunology, 2015Co-Authors: Lin Feng, Weidan Jiang, Pei Wu, Jun Jiang, Shengyao Kuang, Ling Tang, Yongan Zhang, Xiaoqiu ZhouAbstract:This study investigated the effects of dietary valine on Tight Junction Protein transcription, antioxidant status and apoptosis on grass carp gills (Ctenopharyngodon idella). Fish were fed six different experimental diets containing graded levels of valine (4.3, 8.0, 10.6, 13.1, 16.7, 19.1 g/kg). The results indicated that valine deficiency decreased Claudin b, Claudin 3, Occludin and ZO-1 transcription and increased Claudin 15 expression in the fish gill (P 0.05). Valine deficiency also disrupted antioxidant status in the gill by decreasing anti-superoxide radicals and hydroxyl radical capacity, glutathione contents and the activities and mRNA levels of Cu/Zn superoxide dismutase (SOD1), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) (P < 0.05). These results may be ascribed to the down-regulation of NF-E2-related factor 2 (Nrf2), target of rapamycin (TOR) and ribosomal Protein S6 kinase 1 (S6K1) and the up-regulation of Kelch-like-ECH-associated Protein 1 (Keap1) (P < 0.05). Additionally, valine deficiency induced DNA fragmentation via the up-regulation of Caspase 3, Caspase 8 and Caspase 9 expressions (P < 0.05). These results may be ascribed to the improvement in ROS levels in the fish gill (P < 0.05). Taken together, the results showed that valine deficiency impaired the structural integrity of fish gill by disrupted fish antioxidant defenses and regulating the expression of Tight Junction Protein, cytokines, antioxidant enzymes, NF-kappa B p65, I kappa B alpha, TOR, Nrf2, Keap1 and apoptosis-related genes in the fish gill. (C) 2015 Elsevier Ltd. All rights reserved.
Michal Toborek - One of the best experts on this subject based on the ideXlab platform.
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Manufactured Aluminum Oxide Nanoparticles Decrease Expression of Tight Junction Proteins in Brain Vasculature
Journal of Neuroimmune Pharmacology, 2008Co-Authors: Lei Chen, Bernhard Hennig, Robert A. Yokel, Michal ToborekAbstract:Manufactured nanoparticles of aluminum oxide (nano-alumina) have been widely used in the environment; however, their potential toxicity provides a growing concern for human health. The present study focuses on the hypothesis that nano-alumina can affect the blood-brain barrier and induce endothelial toxicity. In the first series of experiments, human brain microvascular endothelial cells (HBMEC) were exposed to alumina and control nanoparticles in dose- and time-responsive manners. Treatment with nano-alumina markedly reduced HBMEC viability, altered mitochondrial potential, increased cellular oxidation, and decreased Tight Junction Protein expression as compared to control nanoparticles. Alterations of Tight Junction Protein levels were prevented by cellular enrichment with glutathione. In the second series of experiments, rats were infused with nano-alumina at the dose of 29 mg/kg and the brains were stained for expression of Tight Junction Proteins. Treatment with nano-alumina resulted in a marked fragmentation and disruption of integrity of claudin-5 and occludin. These results indicate that cerebral vasculature can be affected by nano-alumina. In addition, our data indicate that alterations of mitochondrial functions may be the underlying mechanism of nano-alumina toxicity.
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hiv 1 tat Protein alters Tight Junction Protein expression and distribution in cultured brain endothelial cells
Journal of Neuroscience Research, 2003Co-Authors: Ibolya E Andras, Hong Pu, Maria A Deli, Avindra Nath, Bernhard Hennig, Michal ToborekAbstract:Disruption of the blood-brain barrier (BBB) is widely believed to be the main route of human immunodeficiency virus (HIV) entry into the central nervous system (CNS). Although mechanisms of this process are not fully understood, alterations of Tight Junction Protein expression can contribute, at least in part, to this phenomenon. Tight Junctions are critical structural and functional elements of cerebral microvascular endothelial cells and the BBB. The aim of the present study was to examine the effects of HIV-1 Tat Protein on expression of Tight Junction Proteins. Primary cultures of brain microvascular endothelial cells (BMEC) were employed in these experiments. A 24-hr exposure of BMEC to Tat 1 - 7 2 resulted in a decrease of claudin-1, claudin-5, and zonula occludens (ZO)-2 expression, whereas total levels of occludin and ZO-1 remained unchanged. In addition, a short (3-hr) exposure of BMEC to Tat 1 - 7 2 induced cellular redistribution of claudin-5 immunoreactivity. Tat 1 - 7 2 -induced alterations of claudin-5 expression also were confirmed in vivo where Tat 1 - 7 2 was injected into the right hippocampus of mice. These findings indicate that HIV-1 Tat Protein can markedly affect expression and distribution of specific Tight Junction Proteins in brain endothelium. Alterations of only distinct Tight Junction Proteins suggest a finely tuned effect of Tat 1 - 7 2 on the BBB. Because Tight Junction Proteins are critical for the barrier function of the BBB, such alterations can lead to disturbances of the BBB integrity and contribute to HIV trafficking into the brain.
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HIV‐1 Tat Protein alters Tight Junction Protein expression and distribution in cultured brain endothelial cells
Journal of Neuroscience Research, 2003Co-Authors: Ibolya E Andras, Hong Pu, Maria A Deli, Avindra Nath, Bernhard Hennig, Michal ToborekAbstract:Disruption of the blood-brain barrier (BBB) is widely believed to be the main route of human immunodeficiency virus (HIV) entry into the central nervous system (CNS). Although mechanisms of this process are not fully understood, alterations of Tight Junction Protein expression can contribute, at least in part, to this phenomenon. Tight Junctions are critical structural and functional elements of cerebral microvascular endothelial cells and the BBB. The aim of the present study was to examine the effects of HIV-1 Tat Protein on expression of Tight Junction Proteins. Primary cultures of brain microvascular endothelial cells (BMEC) were employed in these experiments. A 24-hr exposure of BMEC to Tat 1 - 7 2 resulted in a decrease of claudin-1, claudin-5, and zonula occludens (ZO)-2 expression, whereas total levels of occludin and ZO-1 remained unchanged. In addition, a short (3-hr) exposure of BMEC to Tat 1 - 7 2 induced cellular redistribution of claudin-5 immunoreactivity. Tat 1 - 7 2 -induced alterations of claudin-5 expression also were confirmed in vivo where Tat 1 - 7 2 was injected into the right hippocampus of mice. These findings indicate that HIV-1 Tat Protein can markedly affect expression and distribution of specific Tight Junction Proteins in brain endothelium. Alterations of only distinct Tight Junction Proteins suggest a finely tuned effect of Tat 1 - 7 2 on the BBB. Because Tight Junction Proteins are critical for the barrier function of the BBB, such alterations can lead to disturbances of the BBB integrity and contribute to HIV trafficking into the brain.