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PubMed1998

Thrombin-induced vasospasm: cellular signaling mechanisms.

BACKGROUND: In the setting of arterial injury, thrombin contributes to the hemostatic process by activating the coagulation cascade and platelets. We hypothesized that thrombin also contributes to hemostasis by inducing vasospasm. The purpose of this investigation was to characterize the cellular signaling mechanisms that modulate thrombin-induced vascular smooth muscle contractions. METHODS: Contractile responses of intact bovine carotid artery smooth muscles were determined in a muscle bath. Contractile responses were correlated with phosphorylation events as determined with whole cell phosphorylation and two-dimensional gel electrophoresis and with immunoblotting of glycerol-urea or two-dimensional gels. RESULTS: Thrombin (1 to 1000 units/ml) induced sustained vascular smooth muscle contractions of similar magnitude as the potent contractile agonist, endothelin. Thrombin-induced contractions were associated with increases in the phosphorylation of the myosin light chains (MLC20) and in the tyrosine phosphorylation of mitogen-activated protein kinase. CONCLUSIONS: These data suggest that thrombin is a potent physiologic contractile agonist that may modulate some forms of vasospasm. Thrombin-induced contractions are associated with the activation of two cellular signaling pathways, the myosin light chain kinase and the mitogen-activated protein kinase pathways.

Animals↗
PubMed2001

Nongenomic mechanism mediates estradiol stimulation of axon growth in male rat hypothalamic neurons in vitro.

The purpose of the present work was to investigate the participation of estradiol receptors (ER) in estrogen-induced axon growth in vitro. Hypothalamic neurons from 16 day (E16) male rat fetuses were cultured with or without 17-beta-estradiol at 1 x 10(-7) M in basal medium or medium conditioned by astroglia derived from ventral mesencephalon (CM). After 48 hr in vitro, neurite outgrowth was quantified by morphometric analysis. An axogenic effect could be demonstrated for estradiol added to CM. With RT-PCR, the mRNA transcript for ERalpha was found in the donor tissues as well as in the neuron cultures. In this model two specific nuclear ER blockers (tamoxifen and ICI 182,780) were ineffective in blocking the neuritogenic effect, and a membrane-impermeable estrogen-albumin construct (E2-BSA) was as effective as estradiol. These results indicate that the axogenic effect of estradiol at E16 is not exerted through the classical intracellular receptor signal transduction system and suggest the possibility of a membrane-mediated mechanism. The data are discussed in light of our previous findings pointing to the interdependent activation of the estrogenic and the trophic factor signaling pathways that mediate stimulated axon growth.

Animals↗
PubMed1991

Calcium and protein phosphorylation in the transduction of gravity signal in corn roots.

The involvement of calcium and protein phosphorylation in the transduction of gravity signal was studied using corn roots of a light-insensitive variety (Zea mays L., cv. Patriot). The gravitropic response was calcium-dependent. Horizontal placement of roots preloaded with 32P for three minutes resulted in changes in protein phosphorylation of polypeptides of 32 and 35 kD. Calcium depletion resulted in decreased phosphorylation of these phosphoproteins and replenishment of calcium restored the phosphorylation.

Calcium↗
PubMed2001

Adaptation in vertebrate photoreceptors.

When light is absorbed within the outer segment of a vertebrate photoreceptor, the conformation of the photopigment rhodopsin is altered to produce an activated photoproduct called metarhodopsin II or Rh(*). Rh(*) initiates a transduction cascade similar to that for metabotropic synaptic receptors and many hormones; the Rh(*) activates a heterotrimeric G protein, which in turn stimulates an effector enzyme, a cyclic nucleotide phosphodiesterase. The phosphodiesterase then hydrolyzes cGMP, and the decrease in the concentration of free cGMP reduces the probability of opening of channels in the outer segment plasma membrane, producing the electrical response of the cell. Photoreceptor transduction can be modulated by changes in the mean light level. This process, called light adaptation (or background adaptation), maintains the working range of the transduction cascade within a physiologically useful region of light intensities. There is increasing evidence that the second messenger responsible for the modulation of the transduction cascade during background adaptation is primarily, if not exclusively, Ca(2+), whose intracellular free concentration is decreased by illumination. The change in free Ca(2+) is believed to have a variety of effects on the transduction mechanism, including modulation of the rate of the guanylyl cyclase and rhodopsin kinase, alteration of the gain of the transduction cascade, and regulation of the affinity of the outer segment channels for cGMP. The sensitivity of the photoreceptor is also reduced by previous exposure to light bright enough to bleach a substantial fraction of the photopigment in the outer segment. This form of desensitization, called bleaching adaptation (the recovery from which is known as dark adaptation), seems largely to be due to an activation of the transduction cascade by some form of bleached pigment. The bleached pigment appears to activate the G protein transducin directly, although with a gain less than Rh(*). The resulting decrease in intracellular Ca(2+) then modulates the transduction cascade, by a mechanism very similar to the one responsible for altering sensitivity during background adaptation.

Adaptation, Ocular↗
PubMed2005

Signal transduction networks: topology, response and biochemical processes.

Conventionally, biological signal transduction networks are analysed using experimental and theoretical methods to describe specific protein components, interactions, and biochemical processes and to model network behavior under various conditions. While these studies provide crucial information on specific networks, this information is not easily converted to a broader understanding of signal transduction systems. Here, using a specific model of protein interaction we analyse small network topologies to understand their response and general properties. In particular, we catalogue the response for all possible topologies of a given network size to generate a response distribution, analyse the effects of specific biochemical processes on this distribution, and analyse the robustness and diversity of responses with respect to internal fluctuations or mutations in the network. The results show that even three- and four-protein networks are capable of creating diverse and biologically relevant responses, that the distribution of response types changes drastically as a function of biochemical processes at protein level, and that certain topologies strongly pre-dispose a specific response type while others allow for diverse types of responses. This study sheds light on the response types and properties that could be expected from signal transduction networks, provides possible explanations for the role of certain biochemical processes in signal transduction and suggests novel approaches to interfere with signaling pathways at the molecular level. Furthermore it shows that network topology plays a key role on determining response type and properties and that proper representation of network topology is crucial to discover and understand so-called building blocks of large networks.

Animals↗
PubMed1989

Sensory transduction and electrical signaling in guard cells.

Guard cells are a valuable model system for the study of photoreception, ion transport, and osmoregulation in plant cells. Changes in stomatal apertures occur when sensing mechanisms within the guard cells transduce environmental stimull into the ion fluxes and biosynthesis of organic solutes that regulate turgor. The electrical events mediating sensory transduction in guard cells can be characterized with a variety of electrophysiological recording techniques. Recent experiments applying the patch clamp method to guard cell protoplasts have demonstrated activation of electrogenic pumps by blue and red light as well as the presence of potassium channels in guard cell plasmalemma. Light activation of electrogenic proton pumping and the ensuing gating of voltage-dependent ion channels appear to be components of sensory transduction of the stomatal response to light. Mechanisms underlying stomatal control by environmental signals can be understood by studying electrical events associated with ion transport.

Journal Article↗
PubMed1998

cAMP protects endothelial barrier function independent of inhibiting MLC20-dependent tension development.

Exposure of cultured human umbilical vein endothelial cells to the cAMP agonists theophylline and forskolin decreased constitutive isometric tension of a confluent monolayer inoculated on a collagen membrane, but it did not prevent increased tension in cells exposed to thrombin. The inability of cAMP agonists to prevent tension development correlated with an inability of cAMP stimulation to prevent increased 20-kDa myosin light chain (MLC20) phosphorylation in response to thrombin. Although cAMP did not prevent tension development or increased MLC20 phosphorylation, cAMP attenuated the effect of thrombin on transendothelial electrical resistance across a confluent monolayer inoculated on a gold microelectrode. Activation of cAMP-dependent signal transduction did not prevent a decline in resistance in thrombin-treated cells, but it more promptly restored transendothelial resistance to initial basal levels (10 min) compared with thrombin only (60 min). ML-7, an MLC kinase antagonist, at doses that attenuate increased MLC20 phosphorylation and tension development, did not prevent a decline in resistance in thrombin-treated cells. Yet, ML-7 also restored transendothelial resistance more rapidly than thrombin alone (20 min) but at a slower rate than cAMP. These data demonstrate that activation of cAMP-dependent signal transduction protects barrier function independent of inhibition of MLC20-dependent tension development.

Cells, Cultured↗
PubMed2003

Permeabilization in a cerebral endothelial barrier model by pertussis toxin involves the PKC effector pathway and is abolished by elevated levels of cAMP.

Respiratory tract infections caused by Bordetella pertussis are occasionally accompanied by severe neurologic disorders and encephalopathies. For these sequelae to occur the integrity of cerebral barriers needs to be compromised. The influence of pertussis toxin, a decisive virulence factor in the pathogenesis of pertussis disease, on barrier integrity was investigated in model systems for blood-liquor (epithelial) and blood-brain (endothelial) barriers. While pertussis toxin did not influence the barrier function in Plexus chorioideus model systems, the integrity of cerebral endothelial monolayers was severely compromised. Cellular intoxication by pertussis toxin proceeds via ADP-ribosylation of alpha-G(i) proteins, which not only interferes with the homeostatic inhibitory regulation of adenylate cyclase stimulation but also results in a modulation of the membrane receptor coupling. Increasing intra-endothelial cAMP levels by employing cholera toxin or forskolin even inhibited the pertussis toxin-induced permeabilization of endothelial barriers. Therefore, pertussis-toxin-induced permeabilization has to be mediated via a cAMP-independent pathway. To investigate potential signalling pathways we employed several well established cellular drugs activating or inhibiting central effectors of signal transduction pathways, such as phosphatidylinositol 3-kinase, adenylate cyclase, phospholipase C, myosin light chain kinase and protein kinase C. Only inhibitors and activators of protein kinase C and phosphatidylinositol 3-kinase affected the pertussis toxin-induced permeability. In summary, we conclude that permeabilization of cerebral endothelial monolayers by pertussis toxin does not depend on elevated cAMP levels and proceeds via the phosphokinase C pathway.

Animals↗
PubMed1997

Calmodulin regulation of Drosophila light-activated channels and receptor function mediates termination of the light response in vivo.

Calmodulin (CAM) participates in a variety of intracellular transduction processes by modulating signaling molecules in response to calcium changes. We report the characterization of Drosophila Cam mutants and the role of CAM in photoreceptor cell function. Contrary to current models of excitation and TRP channel function, we demonstrate that the transient phenotype of trp mutants can be explained by CAM regulation of the TRPL channel rather than by the loss of a store-operated conductance leading to depletion of the internal stores. We also analyzed light responses in a variety of mutant and transgenic backgrounds and demonstrate the importance of calmodulin in mediating calcium-dependent negative regulation of phototransduction. Our results show that CAM coordinates termination of the light response by modulating receptor and ion channel activity.

Animals↗
PubMed2000

Ultraviolet A radiation-induced biological effects in human skin: relevance for photoaging and photodermatosis.

There is increasing evidence that longwave ultraviolet (UV) radiation (UVA; 320-400 nm) plays an important role in the pathogenesis of photodermatoses such as polymorphous light eruption as well as photoaging. In order to fully understand these detrimental effects it is critical to analyze the photobiological and molecular mechanisms by which UVA radiation affects the function of human skin cells. In this review, our current knowledge about the signal transduction pathway involved in UVA radiation-induced expression of proinflammatory genes relevant to the pathogenesis of polymorphous light eruption will be summarized. In addition, recent studies on the role of mitochondrial DNA mutations in UVA radiation-induced photoaging of human skin will be discussed. For both biological endpoints the UVA radiation-induced generation of singlet oxygen within human skin appears to be of critical importance. These studies are of enormous clinical relevance because they indicate that prevention of the generation of singlet oxygen or inhibition of singlet oxygen-induced signaling pathways may prove to be critical for effective protection of human skin against UVA radiation-induced damage.

Cytokines↗
PubMed2005

Controlling cytokine signaling by constitutive inhibitors.

Cytokines are secreted proteins that regulate diverse biological functions by binding to receptors at the cell surface to activate complex signal transduction pathways including the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. Stringent mechanisms of signal attenuation are essential for ensuring an appropriate, controlled cellular response. Three families of proteins, the SH2-containing phosphatases (SHP), the protein inhibitors of activated STATs (PIAS), and the suppressors of cytokine signaling (SOCS), inhibit specific and distinct aspects of cytokine signal transduction. The analysis of mice lacking genes for members of the SHP has shed much light on the roles of these proteins in vivo. In recent in vitro studies, the protein modifiers ubiquitin and small ubiquitin-like modifier (SUMO) have emerged as key players in the strategies employed by SOCS and PIAS to repress signaling. This review throws light on the mechanisms of action of these regulators as being evolved by the latest researches.

Animals↗
PubMed2001

DFL1, an auxin-responsive GH3 gene homologue, negatively regulates shoot cell elongation and lateral root formation, and positively regulates the light response of hypocotyl length.

A novel dominant mutant designated 'dwarf in light 1' (dfl1-D) was isolated from screening around 1200 Arabidopsis activation-tagged lines. dfl1-D has a shorter hypocotyl under blue, red and far-red light, but not in darkness. Inhibition of cell elongation in shoots caused an exaggerated dwarf phenotype in the adult plant. The lateral root growth of dfl1-D was inhibited without any reduction of primary root length. The genomic DNA adjacent to the right border of T-DNA was cloned by plasmid rescue. The rescued genomic DNA contained a gene encoding a GH3 homologue. The transcript was highly accumulated in the dfl1-D. The dfl1-D phenotype was confirmed by over-expression of the gene in the wild-type plant. The dfl1-D showed resistance to exogenous auxin treatment. Moreover, over-expression of antisense DFL1 resulted in larger shoots and an increase in the number of lateral roots. These results indicate that the gene product of DFL1 is involved in auxin signal transduction, and inhibits shoot and hypocotyl cell elongation and lateral root cell differentiation in light.

Amino Acid Sequence↗
PubMed1997

Attenuation of phytochrome A and B signaling pathways by the Arabidopsis circadian clock.

In higher plants, environmental cues such as light signals are integrated with circadian clock signals to control precisely the daily rhythms observed for many biological functions. We have used a fusion of the promoter of a chlorophyll a/b binding protein gene, CAB2, with firefly luciferase (cab2::luc) to monitor the detailed kinetics of transcription in response to photoreceptor activation in Arabidopsis. Using this marker in phototransduction and circadian-dysfunctional mutants, we studied how signals from phytochrome and the circadian clock are integrated for the regulation of CAB2 transcription. Results from these mutant studies demonstrate that similar expression features, namely, the acute and circadian responses, are present in both etiolated and green seedlings and that the acute and circadian responses are genetically separable. We also demonstrate that persistent Pfr signaling occurs in red light-pulsed etiolated seedlings, which suggests that the circadian clock antagonizes Pfr-mediated signal transduction. Based on these genetic studies, we propose a model for the regulation of CAB2 transcription in which individual photoreceptors and phototransduction components have been assigned to specific pathways for the regulation of discrete kinetic components of the CAB2 expression pattern.

Arabidopsis↗
PubMed1987

Signal transduction in plants: evidence for the involvement of calcium and turnover of inositol phospholipids.

Involvement of calcium and turnover of inositol phospholipids in signal transduction was investigated using roots of a variety of corn (Zea mays L., cv. Merit) which require light to develop gravitropic sensitivity. Depletion of calcium in root tips by EGTA plus calcium ionophore A23187 prior to light treatment resulted in the loss of light-dependent gravisensitivity. Replenishment of calcium to depleted roots restored the light-dependent gravisensitivity. Light treatment of dark-grown roots resulted in an increased level of inositol trisphosphate as compared to controls. Furthermore, 5-hydroxytryptamine, which is known to promote the hydrolysis of phosphoinositides, sensitized dark-grown roots to gravity and increased inositol trisphosphate levels. These results support the hypothesis that calcium and inositol phospholipid turnover play a role in signal transduction in plants.

Calcium↗
PubMed2001

Cyclic AMP-dependent protein kinase A plays a role in the directed migration of human keratinocytes in a DC electric field.

Skin wound healing requires epithelial cell migration for re-epithelialization, wound closure, and re-establishment of normal function. We believe that one of the earliest signals to initiate wound healing is the lateral electric field generated by the wound current. Normal human epidermal keratinocytes migrate towards the negative pole, representing the center of the wound, in direct currents of a physiological strength, 100 mV/mm. Virtually nothing is known about the signal transduction mechanisms used by these cells to sense the endogenous electric field. To elucidate possible protein kinase (PK) involvement in the process, PK inhibitors were utilized. Two important findings have been described. Firstly, addition of 50 nM KT5720, an inhibitor of PKA, resulted in a 53% percent reduction in the directional response of keratinocytes in the electric field, while not significantly affecting general cell motility. The reduction was dose-dependent, there was a gradual decrease in the directional response from 5 to 50 nM. Secondly, addition of 1 microM ML-7, a myosin light chain kinase inhibitor, resulted in an approximate 31% decrease in the distance the cells migrated without affecting directional migration. The PKC inhibitors GF109203X at 4 microM and H-7 at 20 microM and W-7, a CaM kinase inhibitor, did not significantly alter either directed migration or cell migration, although they all resulted in a slight reduction in directional migration. D-erythro-sphingosine at 15 microM, a PKC inhibitor, had virtually no effect on either migration distance or directed migration. These findings demonstrate that divergent kinase signaling pathways regulate general cell motility and sustained directional migration and highlight the complexity of the signal transduction mechanisms involved. The inhibitor studies described in this paper implicate a role for PKA in the regulation of the directional migratory response to applied electric fields, galvanotaxis.

Azepines↗
PubMed1999

Source-sink regulation by sugar and stress.

The regulation of carbon partitioning between source and sink tissues in higher plants is not only important for plant growth and development, but insight into the underlying regulatory mechanism is also a prerequisite to modulating assimilate partitioning in transgenic plants. Hexoses, as well as sucrose, have been recognised as important signal molecules in source-sink regulation. Components of the underlying signal transduction pathways have been identified and parallels, as well as distinct differences, to known pathways in yeast and animals have become apparent. There is accumulating evidence for crosstalk, modulation and integration between signalling pathways responding to phytohormones, phosphate, light, sugars, and biotic and abiotic stress-related stimuli. These complex interactions at the signal transduction levels and co-ordinated regulation of gene expression seem to play a central role in source-sink regulation.

Carbohydrate Metabolism↗
PubMed1995

A novel protein encoded by the InaD gene regulates recovery of visual transduction in Drosophila.

InaDp215 is a point mutation that affects photoreceptor function in Drosophila. To understand the molecular basis of the defect, we isolated the InaD gene and found it encodes a photoreceptor-specific polypeptide of 674 residues. Within its sequence are two repeats that share remarkable homology with a family of cytoskeleton-associated proteins that are involved in signal transduction. Patch-clamp recordings from isolated photoreceptor cells of InaDp215 show a slow deactivation of the light-induced current. This defective deactivation of InaD appears dependent on calcium influx; removal of extracellular calcium masks its abnormal phenotype. Moreover, InaD photoreceptors show increases sensitivity to dim light. We propose that InaD is involved in the negative feedback regulation of the light-activated signaling cascade in Drosophila photoreceptors.

Amino Acid Sequence↗