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  • Articles  (477)
  • Springer  (477)
  • American Chemical Society (ACS)
  • American Geophysical Union
  • Institute of Electrical and Electronics Engineers (IEEE)
  • National Academy of Sciences
  • 2015-2019  (477)
  • 2005-2009
  • 1990-1994
  • 1980-1984
  • 2017  (477)
  • Molecular and Cellular Biochemistry  (136)
  • 6701
  • Biology  (477)
  • Medicine  (477)
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  • Articles  (477)
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  • Springer  (477)
  • American Chemical Society (ACS)
  • American Geophysical Union
  • Institute of Electrical and Electronics Engineers (IEEE)
  • National Academy of Sciences
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  • 2015-2019  (477)
  • 2005-2009
  • 1990-1994
  • 1980-1984
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  • 1
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    CLDN-1 promoted the epithelial to migration and mesenchymal transition (EMT) in human bronchial epithelial cells via Notch pathway (2017)
    Springer
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    Publication Date: 2017-03-19
    Description: Claudin-1 (CLDN-1) is one of main tight junction components that play an important role in epithelial–mesenchymal transition (EMT). However, the effects of CLDN-1 on the migration and EMT induced by TGF-β1 in primary normal human bronchial epithelial (NHBE) and BEAS-2B cells have not been clear. The expression of CLDN-1 was quantified by Western blotting in NHBE and BEAS-2B cells. Cell migration and invasion were detected using transwell assays. The expression level of E-cadherin, N-cadherin, α-SMA, and Vimentin was evaluated by quantitative real-time PCR and Western blotting. Here we showed that the protein expression of CLDN-1 was increased exposed to TGF-β1 in a dose- and time-dependent manner. Knockdown of CLDN-1 using small interfering CLDN-1 RNA (siCLDN-1) prevented the migration and invasion in NHBE and BEAS-2B cells. Moreover, depletion of CLDN-1 promoted the E-cadherin expression and decreased the mRNA and protein levels of N-cadherin, α-SMA, and Vimentin induced by TGF-β1. Furthermore, CLDN-1 silencing resulted in the reduction of the Notch intracellular domain (NICD) and hairy enhancer of split-1 (Hes-1) in mRNA and protein level. Jagged-1, an activator of Notch signaling pathway, abrogated the protective function of siCLDN-1 in migration and EMT. In conclusion, CLDN-1 promoted the migration and EMT through the Notch signaling pathway.
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    Electronic ISSN: 1573-4919
    Topics: Biology , Chemistry and Pharmacology , Medicine
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  • 2
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    Kinetics of expression of genes involved in glucose metabolism after the last meal in overfed mule ducks (2017)
    Springer
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    Publication Date: 2017-03-22
    Description: In waterfowls, overfeeding leads to a hepatic steatosis, also called “foie gras.” We decided to investigate the role of glucose metabolism in steatosis emergence. For this, we measured the expression of genes during the 12 h following the last meal of the overfeeding period. As expected, it showed that the expression of glucose transporter is more precocious in jejunal mucosa, especially for SGLT1, known to be the major transporter at the apical surface. In the liver, GLUT2 and HK1 are upregulated at the same time and seem to work together to import glucose. In peripherals tissues, such as muscle and subcutaneous adipose tissue (SAT), expression of genes of interest occurs later than the one in jejunum and liver. These results are in accordance with the evolution of glycemia. This study allows us to better understand the kinetic treatment of glucose after a meal in overfed ducks. It also will allow researchers to better target their sampling time knowing the optimal point of expression of each gene.
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  • 3
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    The effect and mechanism of dopamine D1 receptors on the proliferation of osteosarcoma cells (2017)
    Springer
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    Publication Date: 2017-02-10
    Description: The physiological and pathological roles of dopamine D1 receptors (DR1) in the regulation of functions in tissues and organs have been recognized. However, whether DR1 are expressed in the osteosarcoma cells and inhibit the proliferation of these cells is unknown. In the present study, we found that DR1 were expressed in the osteosarcoma cells (OS732 cells). SKF-38393 (DR1 agonist) and the overexpression of DR1 decreased the proliferation of OS732 cells; SCH-23390 (DR1 antagonist) and the knockdown of DR1 increased the proliferation of OS732 cells, and both SCH-23390 and the knockdown of DR1 abolished the effect of SKF-38393 on the proliferation of OS732 cells. In addition, SKF-38393 down-regulated the phosphorylation of ERK1/2, PI3K, and Akt; SCH-23390 up-regulated the phosphorylation of ERK1/2, PI3K, and Akt, and SCH-23390 cancelled the effect of SKF-38393. The effect of SKF-38393 on the phosphorylation of ERK1/2, PI3K, and Akt and the proliferation of OS732 cells was similar to PD98059 (an ERK inhibitor) or LY294002 (a PI3K inhibitor), respectively. In conclusion, our results suggest that DR1 are expressed in the osteosarcoma cells and inhibit the proliferation of osteosarcoma cells by the down-regulation of the ERK1/2 and PI3K-Akt pathways. These findings provide a novel target for the treatment of the osteosarcoma.
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  • 4
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    MicroRNA-20b suppresses the expression of ZFP-148 in viral myocarditis (2017)
    Springer
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    Publication Date: 2017-03-01
    Description: Viral myocarditis is a common cardiovascular disease, which seriously endangers the health of people and even leads to sudden unexpected death. MicroRNAs play very important roles in various physical and pathological processes including cardiogenesis and heart diseases. In recent years, miR-20b has been implicated in various diseases such as breast cancer, gastric cancer, hepatocellular carcinoma, cardiovascular diseases. However, the function of miR-20b in the pathological progress of viral myocarditis has not been reported. In this study, we found that miR-20b was up-regulated in mouse heart tissues post Coxsackievirus B3 (CVB3) infection. Bioinformatics analysis identified ZFP-148, a transcription factor that plays essential roles in the regulation of virus replication, is one of the predicted targets of miR-20b. MiR-20b expression was found to be up-regulated and ZFP-148 protein level was markedly repressed during viral myocarditis. Further studies demonstrated that miR-20b directly binds to the 3′-UTR of ZFP-148 and suppresses its translation. Moreover, aberrant expression of miR-20b promoted the expression of anti-apoptosis proteins Bcl-2 and Bcl-xL, suggesting that altered gene expression might promote cardiomyocytes survival in viral myocarditis. Our findings indicated that miR-20b might be a potential therapeutic target for CVB3-induced viral myocarditis and a useful marker for the diagnosis of viral myocarditis.
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  • 5
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    Pyruvate antioxidant roles in human fibroblasts and embryonic stem cells (2017)
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    Publication Date: 2017-03-01
    Description: Oxidative stress has been related to multiple diseases, especially during early embryonic development, when environmental alterations can lead to long-term deleterious effects. In vitro studies of oxidative stress have been mainly focused on somatic cells, but embryonic stem cells (ESCs) represent a promising model of early embryonic development as they are the in vitro equivalent to pluripotent cells in the embryo. Human fibroblasts and ESCs were exposed to different pro-oxidant agents (hydrogen peroxide, tert-butyl hydroperoxide (TBHP), and rotenone) and antioxidants (sodium pyruvate, N-acetylcysteine, Trolox, and sodium selenite) during a 72 h oxidative stress treatment. Then, cell viability, oxidative stress, mitochondrial activity, and gene expression were analyzed, focusing on the antioxidant effect of pyruvate. Pyruvate protected both somatic and pluripotent cells against different pro-oxidant agents, showing strong ROS scavenging capacity, protecting mitochondrial membrane potential, and regulating gene expression and cell metabolism through different mechanisms in fibroblasts and ESCs. In fibroblasts, pyruvate avoided NFKβ nuclear translocation and the upregulation of genes related to the oxidative stress response, while in ESCs pyruvate stimulated the expression of genes involved in anaerobic glycolysis. Fibroblasts and ESCs reacted in different ways to oxidative stress and antioxidant treatment, and pyruvate was the most complete antioxidant, protecting both cell types at different levels.
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  • 6
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    HMGB1 induces endothelial progenitor cells apoptosis via RAGE-dependent PERK/eIF2α pathway (2017)
    Springer
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    Publication Date: 2017-03-03
    Description: Studies have demonstrated that the high-mobility group 1B protein (HMGB1) could regulate endothelial progenitor cell (EPC) homing, but the effect of HMGB1 on EPC apoptosis and associated mechanisms are still unclear. The aim of this study was to investigate the effects of HMGB1 on EPC apoptosis and the possible involvement of the endoplasmic reticulum (ER) stress pathway. EPC apoptosis was determined by flow cytometry. The expressions of PERK, eIF2α, and CHOP were detected by western blotting. Additionally, the effects of PERK shRNA on the biological behaviors of EPCs were assessed. Our results showed that incubation of EPCs with HMGB1 (0.1–1 μg/ml) for 12–48 h induced apoptosis as well as activated ER stress transducers, as assessed by up-regulating PERK protein expression and eIF2α phosphorylation in a dose or time-dependent manner. Moreover, HMGB1-mediated EPC apoptosis and CHOP expression were dramatically suppressed by PERK shRNA or a specific eIF2α inhibitor (salubrinal). Importantly, a blocking antibody specifically targeted against RAGE (anti-RAGE antibody) markedly inhibited HMGB1-induced EPC apoptosis and ER stress marker protein (PERK, eIF2α, and CHOP) expression levels. Our novel findings suggest that HMGB1 triggered EPC apoptosis in a manner of RAGE-mediated activation of the PERK/eIF2α pathway.
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  • 7
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    The role of cytochrome P450 1B1 and its associated mid-chain hydroxyeicosatetraenoic acid metabolites in the development of cardiac hypertrophy induced by isoproterenol (2017)
    Springer
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    Publication Date: 2017-03-03
    Description: Numerous experimental studies have demonstrated the role of cytochrome P450 1B1 (CYP1B1) and its associated mid-chain hydroxyeicosatetraenoic acids (mid-chain HETEs) metabolite in the pathogenesis of cardiac hypertrophy. However, the ability of isoproterenol (ISO) to induce cardiac hypertrophy through mid-chain HETEs has not been investigated yet. Therefore, we hypothesized that ISO induces cardiac hypertrophy through the induction of CYP1B1 and its associated mid-chain HETE metabolites. To test our hypothesis, Sprague–Dawley rats were treated with ISO (5 mg/kg i.p.) for 12 and 72 h whereas, human ventricular cardiomyocytes RL-14 cells were exposed to 100 μM ISO in the presence and absence of 0.5 μM tetramethoxystilbene (TMS) a selective CYP1B1 inhibitor, or 25 nM CYP1B1-siRNA. Moreover, RL-14 cells were transiently transfected with the CRISPR-CYP1B1 plasmid. Thereafter, real-time PCR, western blot analysis, and liquid chromatography–electrospray ionization mass spectroscopy were used to determine the level of gene expression, protein expression, and mid-chain HETEs, respectively. Our results showed that ISO induced CYP1B1 protein expression and the level of cardiac mid-chain HETEs in vivo at pre-hypertrophic and hypertrophic stage. In vitro, inhibition of CYP1B1 using TMS or CYP1B1-siRNA significantly attenuates ISO-induced hypertrophy. Furthermore, overexpression of CYP1B1 significantly induced cellular hypertrophy and mid-chain HETEs metabolite. Mechanistically, the protective effect of TMS against cardiac hypertrophy was mediated through the modulation of superoxide anion, mitogen-activated protein kinases (MAPKs), and nuclear factor-κB (NF-κB). In conclusion, our study provides the first evidence that CYP1B1 and its associated mid-chain HETE metabolites are directly involved in the ISO-induced cardiac hypertrophy.
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  • 8
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    Reversal of endothelial dysfunction in aorta of streptozotocin-nicotinamide-induced type-2 diabetic rats by S-Allylcysteine (2017)
    Springer
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    Publication Date: 2017-03-05
    Description: Dietary measures and plant–based therapies as prescribed by native systems of medicine have gained attraction among diabetics with claims of efficacy. The present study investigated the effects of S-Allylcysteine (SAC) on body weight gain, glucose, insulin, insulin resistance, and nitric oxide synthase in plasma and argininosuccinate synthase (AS) and argininosuccinate lyase (ASL), lipid peroxides and antioxidant enzymes in aorta of control and streptozotocin-nicotinamide (STZ-NA)-induced diabetic rats. Changes in body weight, glucose, insulin, insulin resistance, and antioxidant profiles of aorta and mRNA expressions of nitric oxide synthase, AS, and ASL were observed in experimental rats. SAC (150 mg/kg b.w) showed its therapeutic effects similar to gliclazide in decreasing glucose, insulin resistance, lipid peroxidation, and increasing body weight; insulin, antioxidant enzymes, and mRNA levels of nitric oxide synthase, argininosuccinate synthase, and argininosuccinate lyase genes in STZ-NA rats. Histopathologic studies also revealed the protective nature of SAC on aorta. In conclusion, garlic and its constituents mediate the anti-diabetic potential through mitigating hyperglycemic status, changing insulin resistance by alleviating endothelial dysregulation in both plasma and tissues.
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  • 9
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    Effects of Ganoderma Lucidum shell-broken spore on oxidative stress of the rabbit urinary bladder using an in vivo model of ischemia/reperfusion (2017)
    Springer
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    Publication Date: 2017-05-10
    Description: Oxidative stress plays an important role in specific disease pathophysiology and the aging process. In the history of human kind, many herbs were utilized for disease prevention and anti-aging treatment. However, there are few direct evidences provided by modern laboratory technology. The current study was designed to evaluate Ganoderma Lucidum’s (GL) ability to reduce the damage from in vivo ischemia/reperfusion (I/R) using a rabbit model of I/R that has been effectively utilized to prove the effects of drugs and supplements to reduce oxidative stress. Urinary bladder dysfunction secondary to benign prostatic hyperplasia (BPH) is a major affliction of aging men. One of the major etiologies of obstructive bladder dysfunction (OBD) is oxidative stress induced by I/R. Pharmaceutical studies and clinical research have proven that GL is useful in helping to prevent certain types of pathology and also helpful in prolonging human life in part by acting as an antioxidant. Using an in vivo model of I/R, we have investigated the ability of GL to protect bladder function from oxidative damage mediated by I/R. Our studies demonstrated that ischemia followed by reperfusion resulted in a significant decrease in bladder compliance and decreases in the contractile responses to a variety of forms of contractile stimulation. Pretreatment of rabbits with Ganoderma Lucidum prior to subjecting the rabbits to I/R completely inhibited the negative effects of I/R on both the compliance and contractile responses. These results demonstrate that Ganoderma provides excellent protection of bladder function following I/R (oxidative stress).
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  • 10
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    Thirty-degree shift in optimum temperature of a thermophilic lipase by a single-point mutation: effect of serine to threonine mutation on structural flexibility (2017)
    Springer
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    Publication Date: 2017-05-19
    Description: In order to understand the molecular basis of cold adaptation, we have used directed evolution to transform a thermophilic lipase LipR1 into its psychrophilic counterpart. A single round of random mutagenesis followed by screening for improved variants yielded a mutant with single-point mutation LipR1M1 (S130T), with optimum activity at 20 °C. Its activity at 50 °C is only 20% as compared to wild type (100%). It showed catalytic rate constant ( k cat ) 3 times higher and a catalytic efficiency ( k cat / K m ) 4 times that of wild type. Circular dichroism and fluorescence studies also supported our observation of mutant structural flexibility. Structure analysis using homology models showed that Threonine 130 is exposed to solvent and has lost H-bond interaction with neighboring amino acid, thereby increasing flexibility of this lipase structure.
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