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Differential Activation (differential + activation)
Selected AbstractsDifferential Activation of ERK 1/2 and JNK in Normal Human Fibroblast-like Cells in Response to UVC Radiation Under Different Oxygen Tensions ,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2000Naoki Matsuda ABSTRACT The mechanisms by which mitogen-activated protein kinases (MAPK) respond to the input of UV-induced signal transduction pathways and the resulting biological functions are not well understood. We investigated whether the level of oxygen tension of culture was responsible for the differential activation of MAPK and different cellular outcomes in UVC-irradiated cells. The intracellular oxidative level of normal human fibroblast-like cells in a normal atmosphere (normoxic, 20% O2) was increased within 30 min after UVC irradiation. When cells were cultured at lower oxygen tension in the presence of an antioxidant N -acetyl- l -cysteine (NAC) or under physiologically hypoxic (5% O2) conditions, the elevation of the oxidative level by UV-irradiation was significantly reduced. Among MAPK, extracellular-signal related kinase (ERK) 1/2 was activated by UV regardless of the oxidative level, while c-Jun N-terminal kinase (JNK) activation was inhibited in NAC-treated and in hypoxic cultures. In addition, in cultures at lower oxygen tension, there was less apoptosis and cell survival was enhanced. These results suggest that UV-induced oxidative stress was responsible for intracellular signaling through the JNK pathway. Furthermore, the balance between ERK1/2 and JNK activities after UV irradiation under different oxygen tensions possibly modified cellular outcome in response to UV. [source] ORIGINAL ARTICLE: Haplotype-dependent Differential Activation of the Human IL-10 Gene Promoter in Macrophages and Trophoblasts: Implications for Placental IL-10 Deficiency and Pregnancy ComplicationsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010Surendra Sharma Citation Sharma S, Stabila J, Pietras L, Singh AR, McGonnigal B, Ernerudh J, Matthiesen L, Padbury JF. Haplotype-dependent differential activation of the human IL-10 gene promoter in macrophages and trophoblasts: Implications for placental IL-10 deficiency and pregnancy complications. Am J Reprod Immunol 2010; 64: 179,187 Problem, Polymorphic changes in the IL-10 gene promoter have been identified that lead to altered IL-10 production. We hypothesized that because of these genotypic changes, the IL-10 promoter might be expressed in a cell type,specific manner and may respond differentially to inflammatory triggers. Method of study, We created reporter gene promoter constructs containing GCC, ACC, and ATA haplotypes using DNA from patients harboring polymorphic changes at ,1082 (G,A), ,819 (C,T), and ,592 (C,A) sites in the IL-10 promoter. These individual luciferase reporter constructs were transiently transfected into either primary term trophoblasts or THP1 monocytic cells. DNA-binding studies were performed to implicate the role of the Sp1 transcription factor in response to differential promoter activity. Results, Our results suggest that the GCC promoter construct was activated in trophoblast cells in response to lipopolysaccharide (LPS), as demonstrated by reporter gene expression, but not in monocytic cells. The ACC construct showed weaker activation in both cell types. Importantly, while the ATA promoter was constitutively activated in both cell types, its expression was selectively repressed in response to LPS, but only in trophoblasts. DNA-nuclear protein binding assays with nuclear extracts from LPS treated or untreated cells suggested a functional relevance for Sp1 binding differences at the ,592 position. Conclusions, These results demonstrate cell type,specific effects of the genotypic changes in the IL-10 gene promoter. These responses may be further modulated by bacterial infections or other inflammatory conditions to suppress IL-10 production in human trophoblasts. [source] Rollvection versus linearvection: Comparison of brain activations in PETHUMAN BRAIN MAPPING, Issue 3 2004Angela Deutschländer Abstract We conducted a PET study to directly compare the differential effects of visual motion stimulation that induced either rollvection about the line of sight or forward linearvection along this axis in the same subjects. The main question was, whether the areas that respond to vection are identical or separate and distinct for rollvection and linearvection. Eleven healthy volunteers were exposed to large-field (100° × 60°) visual motion stimulation consisting of (1) dots accelerating from a focus of expansion to the edge of the screen (forward linearvection) and (2) dots rotating counterclockwise in the frontal plane (clockwise rollvection). These two stimuli, which induced apparent self-motion in all subjects, were compared to each other and to a stationary visual pattern. Linearvection and rollvection led to bilateral activations of visual areas including medial parieto-occipital (PO), occipito-temporal (MT/V5), and ventral occipital (fusiform gyri) cortical areas, as well as superior parietal sites. Activations in the polar visual cortex around the calcarine sulcus (BA 17, BA 18) were larger and more significant during linearvection. Temporo-parietal sites displayed higher activity levels during rollvection. Differential activation of PO or MT/V5 was not found. Both stimuli led to simultaneous deactivations of retroinsular regions (more pronounced during linearvection); this is compatible with an inhibitory interaction between the visual and the vestibular systems for motion perception. Hum. Brain Mapp. 21:143,153, 2004. © 2004 Wiley-Liss, Inc. [source] Differential activation of stress-responsive signalling proteins associated with altered loading in a rat skeletal muscleJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2005Inho Choi Abstract Skeletal muscle undergoes a significant reduction in tension upon unloading. To explore intracellular signalling mechanisms underlying this phenomenon, we investigated twitch tension, the ratio of actin/myosin filaments, and activities of key signalling molecules in rat soleus muscle during a 3-week hindlimb suspension and 2-week reloading. Twitch tension and myofilament ratio (actin/myosin) gradually decreased during unloading but progressively recovered to initial levels during reloading. To study the involvement of stress-responsive signalling proteins during these changes, the activities of protein kinase C alpha (PKC,) and three mitogen-activated protein kinases (MAPKs),c-Jun NH2 -terminal kinase (JNK), extracellular signal-regulated protein kinase (ERK), and p38 MAPK,were examined using immunoblotting and immune complex kinase assays. PKC, phosphorylation correlated positively with the tension (Pearson's r,=,0.97, P,<,0.001) and the myofilament ratio (r,=,0.83, P,<,0.01) over the entire unloading and reloading period. Treatment of the soleus muscle with a PKC activator resulted in a similar paralleled increment in both PKC, phosphorylation and the ,-sarcomeric actin expression. The three MAPKs differed in the pattern of activation in that JNK activity peaked only for the first hours of reloading, whereas ERK and p38 MAPK activities remained elevated during reloading. These results suggest that PKC, may play a pivotal role in converting loading stress to intracellular changes in contractile proteins that determine muscle tension. Differential activation of MAPKs may also help alleviate muscle damage, modulate energy transport and/or regulate the expression of contractile proteins upon altered loading. J. Cell. Biochem. © 2005 Wiley-Liss, Inc. [source] Adrenergic regulation of cardiac myocyte apoptosisJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2001Krishna Singh The direct effects of catecholamines on cardiac myocytes may contribute to both normal physiologic adaptation and pathologic remodeling, and may be associated with cellular hypertrophy, apoptosis, and alterations in contractile function. Norepinephrine (NE) signals via ,- and ,-adrenergic receptors (AR) that are coupled to G-proteins. Pharmacologic studies of cardiac myocytes in vitro demonstrate that stimulation of ,1 -AR induces apoptosis which is cAMP-dependent and involves the voltage-dependent calcium influx channel. In contrast, stimulation of ,2 -AR exerts an anti-apoptotic effect which appears to be mediated by a pertussis toxin-sensitive G protein. Stimulation of ,1 -AR causes myocyte hypertrophy and may exert an anti-apoptotic action. In transgenic mice, myocardial overexpression of either ,1 -AR or G,s is associated with myocyte apoptosis and the development of dilated cardiomyopathy. Myocardial overexpression of ,2 -AR at low levels results in improved cardiac function, whereas expression at high levels leads to dilated cardiomyopathy. Overexpression of wildtype ,1B -AR does not result in apoptosis, whereas overexpression of G,q results in myocyte hypertrophy and/or apoptosis depending on the level of expression. Differential activation of the members of the mitogen-activated protein kinase (MAPK) superfamily and production of reactive oxygen species appear to play a key role in mediating the actions of adrenergic pathways on myocyte apoptosis and hypertrophy. This review summarizes current knowledge about the molecular and cellular mechanisms involved in the regulation of cardiac myocyte apoptosis via stimulation of adrenergic receptors and their coupled effector pathways. © 2001 Wiley-Liss, Inc. [source] Differential activation of C1 complement components in rat spinal cord after sciatic nerve injuryJOURNAL OF NEUROCHEMISTRY, Issue 2003J. Mika Neuroimmune interactions are discussed to drive neuropathic pain. We used the Bennett model to correlate pain and cellular expression profiles of the complement factors C1q and C1q-associated serine proteases C1r/C1s in lumbar spinal cord. At 2 days C1q mRNA levels increased ipsilateral to the lesion, and peaked at 8 days when allodynia and severe walking problems were present. During regeneration walking problems disappeared together with C1q mRNA levels. C1q biosynthesis was restricted to microglia. Surprisingly, C1s/C1r biosynthesis was not increased after injury suggesting a role for C1q different from classical complement activation. Sustained C1q expression in spinal microglia after lesion in conjunction with pain behavior indicates that microglial C1q may be causally involved in the development and maintenance of neuropathic pain. Acknowledgements:, Supported by BMBF01GG9818, SFB297, DFGWE910/8-3, KBN3P05C00623. [source] Involvement of the human frontal eye field and multiple parietal areas in covert visual selection during conjunction searchEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2000Tobias Donner Abstract Searching for a target object in a cluttered visual scene requires active visual attention if the target differs from distractors not by elementary visual features but rather by a feature conjunction. We used functional magnetic resonance imaging (fMRI) in human subjects to investigate the functional neuroanatomy of attentional mechanisms employed during conjunction search. In the experimental condition, subjects searched for a target defined by a conjunction of colour and orientation. In the baseline condition, subjects searched for a uniquely coloured target, regardless of its orientation. Eye movement recordings outside the scanner verified subjects' ability to maintain fixation during search. Reaction times indicated that the experimental condition was attentionally more demanding than the baseline condition. Differential activations between conditions were therefore ascribed to top-down modulation of neural activity. The frontal eye field, the ventral precentral sulcus and the following posterior parietal regions were consistently activated: (i) the postcentral sulcus; (ii) the posterior; and (iii) the anterior part of the intraparietal sulcus; and (iv) the junction of the intraparietal with the transverse occipital sulcus. Parietal regions were spatially distinct and displayed differential amplitudes of signal increase with a maximal amplitude in the posterior intraparietal sulcus. Less consistent activation was found in the lateral fusiform gyrus. These results suggest an involvement of the human frontal eye field in covert visual selection of potential targets during search. These results also provide evidence for a subdivision of posterior parietal cortex in multiple areas participating in covert visual selection, with a major contribution of the posterior intraparietal sulcus. [source] Efficient help for autoreactive B-cell activation requires CD4+ T-cell recognition of an agonist peptide at the effector stageEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 9 2009Brian D. Hondowicz Abstract T-cell recognition of peptide/MHC complexes is flexible and can lead to differential activation, but how interactions with agonist (full activation) or partial agonist (suboptimal activation) peptides can shape immune responses in vivo is not well characterized. We investigated the effect of stimulation by agonist or partial agonist ligands during initial CD4+ T-cell priming, and subsequent T-B-cell cognate interactions, on antibody production by anti-chromatin B cells. We found that autoantibody production required TCR recognition of an agonist peptide at the effector stage of B-cell activation. However, interaction with a weak agonist ligand at this effector stage failed to promote efficient autoantibody production, even if the CD4+ T cells were fully primed by an agonist peptide. These studies suggest that the reactivity of the TCR for a target self-peptide during CD4+ T-B-cell interaction can be a critical determinant in restraining anti-chromatin autoantibody production. [source] Antero-posterior activity changes in the superficial masseter muscle after exposure to experimental painEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 2 2002Jens C. Türp The aim of this randomized, controlled, double-blind study was to examine how the activation pattern of the masseter muscle changes during natural function when experimental pain is induced in a discrete anterior area of the muscle. In 20 subjects, three bipolar surface electrodes and three intramuscular fine-wire electrodes (antero-posterior mapping) were simultaneously attached above and in the right masseter muscle to record the electromyographic (EMG) activity during unilateral chewing before and after infusion of a 0.9% isotonic and 5% hypertonic saline bolus in the anterior area of the muscle. The activity of the contralateral masseter muscle was registered by surface electrodes. In addition, the development of pain intensity was quantitatively measured with a numerical rating scale (NRS). While both saline concentrations caused pain, the hypertonic solution evoked stronger pain. The experiments also provided evidence of a significant although differential activity reduction of the ipsilateral masseter muscle in the antero-posterior direction. The activity reduction decreased with increasing distance from the location of the infusion. The results support the idea that the strategy of differential activation protects the injured muscle while simultaneously maintaining optimal function. [source] Adaptive tolerance to oxidative stress and the induction of antioxidant enzymatic activities in Candida albicans are independent of the Hog1 and Cap1-mediated pathwaysFEMS YEAST RESEARCH, Issue 6 2010Pilar Gónzalez-Pįrraga Abstract In the pathogenic yeast Candida albicans, the MAP-kinase Hog1 mediates an essential protective role against oxidative stress, a feature shared with the transcription factor Cap1. We analysed the adaptive oxidative response of strains with both elements altered. Pretreatment with gentle doses of oxidants or thermal upshifts (28,37 and 37,42 °C) improved survival in the face of high concentrations of oxidants (50 mM H2O2 or 40 mM menadione), pointing to a functional cross-protective mechanism in the mutants. The oxidative challenge promoted a marked intracellular synthesis of trehalose, although hog1 (but not cap1) cells always displayed high basal trehalose levels. Hydrogen peroxide (H2O2) induced mRNA expression of the trehalose biosynthetic genes (TPS1 and TPS2) in the tested strains. Furthermore, oxidative stress also triggered a differential activation of various antioxidant activities, whose intensity was greater after HOG1 and CAP1 deletion. The pattern of activity was dependent on the oxidant dosage applied: low concentrations of H2O2 (0.5,5 mM) clearly induced catalase and glutathione reductase (GR), whereas drastic H2O2 exposure (50 mM) increased Mn-superoxide dismutase (SOD) isozyme-mediated SOD activity. These results firmly support the existence in C. albicans of both Hog1- and Cap1-independent mechanisms against oxidative stress. [source] Hypoxia modulates cholinergic but not opioid activation of G proteins in rat hippocampusHIPPOCAMPUS, Issue 10 2007V.S. Hambrecht Abstract Intermittent hypoxia, such as that associated with obstructive sleep apnea, can cause neuronal death and neurobehavioral dysfunction. The cellular and molecular mechanisms through which hypoxia alter hippocampal function are incompletely understood. This study used in vitro [35S]guanylyl-5,- O -(,-thio)-triphosphate ([35S]GTP,S) autoradiography to test the hypothesis that carbachol and DAMGO activate hippocampal G proteins. In addition, this study tested the hypothesis that in vivo exposure to different oxygen (O2) concentrations causes a differential activation of G proteins in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus. G protein activation was quantified as nCi/g tissue in CA1, CA3, and DG from rats housed for 14 days under one of three different oxygen conditions: normoxic (21% O2) room air, or hypoxia (10% O2) that was intermittent or sustained. Across all regions of the hippocampus, activation of G proteins by the cholinergic agonist carbachol and the mu opioid agonist [D-Ala2, N-Met-Phe4, Gly5] enkephalin (DAMGO) was ordered by the degree of hypoxia such that sustained hypoxia > intermittent hypoxia > room air. Carbachol increased G protein activation during sustained hypoxia (38%), intermittent hypoxia (29%), and room air (27%). DAMGO also activated G proteins during sustained hypoxia (52%), intermittent hypoxia (48%), and room air (43%). Region-specific comparisons of G protein activation revealed that the DG showed significantly less activation by carbachol following intermittent hypoxia and sustained hypoxia than the CA1. Considered together, the results suggest the potential for hypoxia to alter hippocampal function by blunting the cholinergic activation of G proteins within the DG. © 2007 Wiley-Liss, Inc. [source] Individual sensitivity to pain expectancy is related to differential activation of the hippocampus and amygdalaHUMAN BRAIN MAPPING, Issue 2 2010Michal Ziv Abstract Anxiety arising during pain expectancy can modulate the subjective experience of pain. However, individuals differ in their sensitivity to pain expectancy. The amygdale and hippocampus were proposed to mediate the behavioral response to aversive stimuli. However, their differential role in mediating anxiety-related individual differences is not clear. Using fMRI, we investigated brain activity during expectancy to cued or uncued thermal pain applied to the wrist. Following each stimulation participants rated the intensity of the painful experience. Activations in the amygdala and hippocampus were examined with respect to individual differences in harm avoidance (HA) personality trait, and individual sensitivity to expectancy, (i.e. response to cued vs. uncued painful stimuli). Only half of the subjects reported on cued pain as being more painful than uncued pain. In addition, we found a different activation profile for the amygdala and hippocampus during pain expectancy and experience. The amygdala was more active during expectancy and this activity was correlated with HA scores. The hippocampal activity was equally increased during both pain expectancy and experience, and correlated with the individual's sensitivity to expectancy. Our findings suggest that the amygdala supports an innate tendency to approach or avoid pain as reflected in HA trait, whereas the hippocampus mediates the effect of context possibly via appraisal of the stimulus value. Hum Brain Mapp, 2010. © 2009 Wiley-Liss, Inc. [source] Covariations among fMRI, skin conductance, and behavioral data during processing of concealed informationHUMAN BRAIN MAPPING, Issue 12 2007Matthias Gamer Abstract Imaging techniques have been used to elucidate the neural correlates that underlie deception. The scientifically best understood paradigm for the detection of deception, however, the guilty knowledge test (GKT), was rarely used in imaging studies. By transferring a GKT-paradigm to a functional magnetic resonance imaging (fMRI) study, while additionally quantifying reaction times and skin conductance responses (SCRs), this study aimed at identifying the neural correlates of the behavioral and electrodermal response pattern typically found in GKT examinations. Prior to MR scanning, subjects viewed two specific items (probes) and were instructed to hide their knowledge of these. Two other specific items were designated as targets and required a different behavioral response during the experiment and eight items served as irrelevant stimuli. Reaction times and SCR amplitudes differed significantly between all three item types. The neuroimaging data revealed that right inferior frontal and mid-cingulate regions were more active for probe and target trials compared to irrelevants. Moreover, the differential activation in the right inferior frontal region was modulated by stimulus conflicts. These results were interpreted as an increased top-down influence on the stimulus-response-mapping for concealed and task-relevant items. Additionally, the influence of working memory and retrieval processes on this activation pattern is discussed. Using parametric analyses, reaction times and SCR amplitudes were found to be linearly related to activity in the cerebellum, the right inferior frontal cortex, and the supplementary motor area. This result provides a first link between behavioral measures, sympathetic arousal, and neural activation patterns during a GKT examination. Hum Brain Mapp 2007. © 2007 Wiley-Liss, Inc. [source] Event-Related fMRI of Inhibitory Control in the Predominantly Inattentive and Combined Subtypes of ADHDJOURNAL OF NEUROIMAGING, Issue 3 2009Mary V. Solanto PhD ABSTRACT BACKGROUND AND PURPOSE To examine the neurophysiological basis for the pronounced differences in hyperactivity and impulsiveness that distinguish the predominantly inattentive type of attention-deficit/hyperactivity disorder (ADHD-PI) from the combined type of the disorder (ADHD-C). METHODS Event-related brain responses to a go/no-go test of inhibitory control were measured with functional magnetic resonance imaging (fMRI) in 11 children with ADHD-C and 9 children with ADHD-PI, aged 7 to 13 years, who were matched for age, sex, and intelligence. RESULTS There were no significant group differences in task performance. Children with ADHD-C and ADHD-PI activated overlapping regions of right inferior frontal gyrus, right superior temporal lobe, and left inferior parietal lobe during inhibitory control. However, the magnitude of the activation in the temporal and parietal regions, as well as in the bilateral middle frontal gyrus, was greater in children with ADHD-PI than those with ADHD-C. Conversely, children with ADHD-C activated bilateral medial occipital lobe to a greater extent than children with ADHD-PI. CONCLUSIONS The results provide preliminary evidence that phenotypic differences between the ADHD-C and ADHD-PI subtypes are associated with differential activation of regions that have previously been implicated in the pathophysiology of ADHD and are thought to mediate executive and attentional processes. [source] Differential activity patterns in the masseter muscle under simulated clenching and grinding forcesJOURNAL OF ORAL REHABILITATION, Issue 8 2005H. J. SCHINDLER summary, The aim of this study was to investigate (i) whether the masseter muscle shows differential activation under experimental conditions which simulate force generation during clenching and grinding activities; and (ii) whether there are (a) preferentially active muscle regions or (b) force directions which show enhanced muscle activation. To answer these questions, the electromyographic (EMG) activity of the right masseter muscle was recorded with five intramuscular electrodes placed in two deep muscle areas and in three surface regions. Intraoral force transfer and force measurement were achieved by a central bearing pin device equipped with three strain gauges (SG). The activity distribution in the muscle was recorded in four different mandibular positions (central, left, right, anterior). In each position, maximum voluntary contraction (MVC) was exerted in vertical, posterior, anterior, medial and lateral directions. The investigated muscle regions showed different amount of EMG activity. The relative intensity of the activation, with respect to other regions, changed depending on the task. In other words, the muscle regions demonstrated heterogeneous changes of the EMG pattern for the various motor tasks. The resultant force vectors demonstrated similar amounts in all horizontal bite directions. Protrusive force directions revealed the highest relative activation of the masseter muscle. The posterior deep muscle region seemed to be the most active compartment during the different motor tasks. The results indicate a heterogeneous activation of the masseter muscle under test conditions simulating force generation during clenching and grinding. Protrusively directed bite forces were accompanied by the highest activation in the muscle, with the posterior deep region as the most active area. [source] N -methyl-d-aspartate Receptor Responses Are Differentially Modulated by Noncompetitive Receptor Antagonists and Ethanol in Inbred Long-Sleep and Short-Sleep Mice: Behavior and ElectrophysiologyALCOHOLISM, Issue 12 2000Taleen Hanania Background: Short-sleep (SS) mice exhibit higher locomotor activity than do long-sleep (LS) mice when injected with low doses of ethanol or the noncompetitive N -methyl-D-aspartate receptor (NMDAR) antagonist MK-801 (dizocilpine). SS mice also have higher densities of brain NMDARs. However, two strains of LS X SS recombinant inbred (RI) mice also show differential activation to ethanol and MK-801, but have similar numbers of NMDARs. Here we used inbred LS (ILS) and SS (ISS) mice to investigate further the relationship between NMDARs and sensitivity to the stimulant effects of low doses of ethanol. Methods: Open field activity and spontaneous alternations were measured after saline or drug injection. [3H]MK-801 binding parameters were determined in hippocampus, cortex, striatum, and nucleus accumbens. Extracellular field excitatory postsynaptic potentials (fEPSPs) were recorded in the CA1 region of hippocampal slices. Results: Systemic injection of either ethanol or MK-801 increased locomotor activity to a greater extent in ISS mice than in ILS mice. The competitive NMDAR antagonist 2-carboxypiperazin-4-yl-propyl-1,1phosphonic acid (±CPP) depressed activity of ILS, but not ISS, mice. No strain differences were observed in spontaneous alternations or in the number or affinity of NMDARs in the brain regions examined. Likewise, the magnitudes of hippocampal NMDAR-mediated fEPSPs were similar in ILS and ISS mice and were inhibited to the same extent by a competitive NMDAR antagonist. However, both ethanol and the NMDAR NR2B receptor antagonist ifenprodil inhibited the late component of hippocampal NMDAR fEPSPs to a greater extent in ISS, than in ILS, mice. Conclusions: Differential ethanol- and MK-801-induced behavioral activation in ILS and ISS mice was not associated with differences in NMDAR number. Nonetheless, pharmacological differences in hippocampal NMDAR responsiveness suggest that ISS mice express NMDARs that have a greater sensitivity to noncompetitive, but not competitive, NMDAR antagonists. These differences, which may reflect differences in NMDAR subunit composition, could underlie the differential responsiveness to low doses of ethanol in ILS and ISS mice. [source] Multiple histidine kinases regulate entry into stationary phase and sporulation in Bacillus subtilisMOLECULAR MICROBIOLOGY, Issue 3 2000Min Jiang Protein homology studies identified five kinases potentially capable of phosphorylating the Spo0F response regulator and initiating sporulation in Bacillus subtilis. Two of these kinases, KinA and KinB, were known from previous studies to be responsible for sporulation in laboratory media. In vivo studies of the activity of four of the kinases, KinA, KinC, KinD (ykvD) and KinE (ykrQ), using abrB transcription as an indicator of Spo0A,P level, revealed that KinC and KinD were responsible for Spo0A,P production during the exponential phase of growth in the absence of KinA and KinB. In vitro, all four kinases dephosphorylated Spo0F,P with the production of ATP at approximately the same rate, indicating that they possess approximately equal affinity for Spo0F. All the kinases were expressed during growth and early stationary phase, suggesting that the differential activity observed in growth and sporulation results from differential activation by signal ligands unique to each kinase. [source] Differential Activation of ERK 1/2 and JNK in Normal Human Fibroblast-like Cells in Response to UVC Radiation Under Different Oxygen Tensions ,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2000Naoki Matsuda ABSTRACT The mechanisms by which mitogen-activated protein kinases (MAPK) respond to the input of UV-induced signal transduction pathways and the resulting biological functions are not well understood. We investigated whether the level of oxygen tension of culture was responsible for the differential activation of MAPK and different cellular outcomes in UVC-irradiated cells. The intracellular oxidative level of normal human fibroblast-like cells in a normal atmosphere (normoxic, 20% O2) was increased within 30 min after UVC irradiation. When cells were cultured at lower oxygen tension in the presence of an antioxidant N -acetyl- l -cysteine (NAC) or under physiologically hypoxic (5% O2) conditions, the elevation of the oxidative level by UV-irradiation was significantly reduced. Among MAPK, extracellular-signal related kinase (ERK) 1/2 was activated by UV regardless of the oxidative level, while c-Jun N-terminal kinase (JNK) activation was inhibited in NAC-treated and in hypoxic cultures. In addition, in cultures at lower oxygen tension, there was less apoptosis and cell survival was enhanced. These results suggest that UV-induced oxidative stress was responsible for intracellular signaling through the JNK pathway. Furthermore, the balance between ERK1/2 and JNK activities after UV irradiation under different oxygen tensions possibly modified cellular outcome in response to UV. [source] Co-occurring increases of calcium and organellar reactive oxygen species determine differential activation of antioxidant and defense enzymes in Ulva compressa (Chlorophyta) exposed to copper excessPLANT CELL & ENVIRONMENT, Issue 10 2010ALBERTO GONZALEZ ABSTRACT In order to analyse copper-induced calcium release and (reactive oxygen species) ROS accumulation and their role in antioxidant and defense enzymes activation, the marine alga Ulva compressa was exposed to 10 µM copper for 7 d. The level of calcium, extracellular hydrogen peroxide (eHP), intracellular hydrogen peroxide (iHP) and superoxide anions (SA) as well as the activities of ascorbate peroxidase (AP), glutathione reductase (GR), glutathione-S-transferase (GST), phenylalanine ammonia lyase (PAL) and lipoxygenase (LOX) were determined. Calcium release showed a triphasic pattern with peaks at 2, 3 and 12 h. The second peak was coincident with increases in eHP and iHP and the third peak with the second increase of iHP. A delayed wave of SA occurred after day 3 and was not accompanied by calcium release. The accumulation of iHP and SA was mainly inhibited by organellar electron transport chains inhibitors (OETCI), whereas calcium release was inhibited by ryanodine. AP activation ceased almost completely after the use of OETCI. On the other hand, GR and GST activities were partially inhibited, whereas defense enzymes were not inhibited. In contrast, PAL and LOX were inhibited by ryanodine, whereas AP was not inhibited. Thus, copper stress induces calcium release and organellar ROS accumulation that determine the differential activation of antioxidant and defense enzymes. [source] Memory-based or afferent processes in mismatch negativity (MMN): A review of the evidencePSYCHOPHYSIOLOGY, Issue 1 2005Risto Näätänen Abstract The mismatch negativity (MMN) is an electromagnetic response to any discriminable change in regular auditory input. This response is usually interpreted as being generated by an automatic cortical change-detection process in which a difference is found between the current input and the representation of the regular aspects of the preceding auditory input. Recently, this interpretation was questioned by Jääskeläinen et al. (2004) who proposed that the MMN is a product of an N1 (N1a) difference wave emerging in the subtraction procedure used to visualize and quantify the MMN. We now evaluate this "adaptation hypothesis" of the MMN in the light of the available data. It is shown that the MMN cannot be accounted for by differential activation of the afferent N1 transient detectors by repetitive ("standard") stimuli and deviant ("novel") stimuli and that the presence of a memory representation of the standard is required for the elicitation of MMN. [source] ORIGINAL ARTICLE: Haplotype-dependent Differential Activation of the Human IL-10 Gene Promoter in Macrophages and Trophoblasts: Implications for Placental IL-10 Deficiency and Pregnancy ComplicationsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010Surendra Sharma Citation Sharma S, Stabila J, Pietras L, Singh AR, McGonnigal B, Ernerudh J, Matthiesen L, Padbury JF. Haplotype-dependent differential activation of the human IL-10 gene promoter in macrophages and trophoblasts: Implications for placental IL-10 deficiency and pregnancy complications. Am J Reprod Immunol 2010; 64: 179,187 Problem, Polymorphic changes in the IL-10 gene promoter have been identified that lead to altered IL-10 production. We hypothesized that because of these genotypic changes, the IL-10 promoter might be expressed in a cell type,specific manner and may respond differentially to inflammatory triggers. Method of study, We created reporter gene promoter constructs containing GCC, ACC, and ATA haplotypes using DNA from patients harboring polymorphic changes at ,1082 (G,A), ,819 (C,T), and ,592 (C,A) sites in the IL-10 promoter. These individual luciferase reporter constructs were transiently transfected into either primary term trophoblasts or THP1 monocytic cells. DNA-binding studies were performed to implicate the role of the Sp1 transcription factor in response to differential promoter activity. Results, Our results suggest that the GCC promoter construct was activated in trophoblast cells in response to lipopolysaccharide (LPS), as demonstrated by reporter gene expression, but not in monocytic cells. The ACC construct showed weaker activation in both cell types. Importantly, while the ATA promoter was constitutively activated in both cell types, its expression was selectively repressed in response to LPS, but only in trophoblasts. DNA-nuclear protein binding assays with nuclear extracts from LPS treated or untreated cells suggested a functional relevance for Sp1 binding differences at the ,592 position. Conclusions, These results demonstrate cell type,specific effects of the genotypic changes in the IL-10 gene promoter. These responses may be further modulated by bacterial infections or other inflammatory conditions to suppress IL-10 production in human trophoblasts. [source] Exercise intensity-dependent regulation of peroxisome proliferator-activated receptor , coactivator-1, mRNA abundance is associated with differential activation of upstream signalling kinases in human skeletal muscleTHE JOURNAL OF PHYSIOLOGY, Issue 10 2010Brendan Egan Skeletal muscle contraction increases intracellular ATP turnover, calcium flux, and mechanical stress, initiating signal transduction pathways that modulate peroxisome proliferator-activated receptor , coactivator-1, (PGC-1,)-dependent transcriptional programmes. The purpose of this study was to determine if the intensity of exercise regulates PGC-1, expression in human skeletal muscle, coincident with activation of signalling cascades known to regulate PGC-1, transcription. Eight sedentary males expended 400 kcal (1674 kj) during a single bout of cycle ergometer exercise on two separate occasions at either 40% (LO) or 80% (HI) of,. Skeletal muscle biopsies from the m. vastus lateralis were taken at rest and at +0, +3 and +19 h after exercise. Energy expenditure during exercise was similar between trials, but the high intensity bout was shorter in duration (LO, 69.9 ± 4.0 min; HI, 36.0 ± 2.2 min, P < 0.05) and had a higher rate of glycogen utilization (P < 0.05). PGC-1, mRNA abundance increased in an intensity-dependent manner +3 h after exercise (LO, 3.8-fold; HI, 10.2-fold, P < 0.05). AMP-activated protein kinase (AMPK) (2.8-fold, P < 0.05) and calcium/calmodulin-dependent protein kinase II (CaMKII) phosphorylation (84%, P < 0.05) increased immediately after HI but not LO. p38 mitogen-activated protein kinase (MAPK) phosphorylation increased after both trials (,2.0-fold, P < 0.05), but phosphorylation of the downstream transcription factor, activating transcription factor-2 (ATF-2), increased only after HI (2.4-fold, P < 0.05). Cyclic-AMP response element binding protein (CREB) phosphorylation was elevated at +3 h after both trials (,80%, P < 0.05) and class IIa histone deacetylase (HDAC) phosphorylation increased only after HI (2.0-fold, P < 0.05). In conclusion, exercise intensity regulates PGC-1, mRNA abundance in human skeletal muscle in response to a single bout of exercise. This effect is mediated by differential activation of multiple signalling pathways, with ATF-2 and HDAC phosphorylation proposed as key intensity-dependent mediators. [source] | |||||||||||||||||||||||||