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At least 415 records · Page 23Linked to original sources
PubMed2006

Differential localization of unconventional myosin I and nonmuscle myosin II during B cell spreading.

Cross-linking of CD44 in vitro promotes chemokinesis and actin-based dendrite formation in T and B cells. However, the mechanisms by which the adhesion molecule CD44 induces cytoskeleton activation in lymphocytes are still poorly understood. In this study, we have investigated whether myosin isoforms are involved in CD44-dependent dendrite formation in activated B cells. Pharmacological inhibition of myosin with 2,3-butanedione monoxime strongly affected spreading and dendrite formation, suggesting that these cellular motors may participate in these phenomena. Furthermore, immunofluorescence analysis showed differences in subcellular localization of class I and class II myosin during B cell spreading. In response to CD44 cross-linking, myosin-1c was polarized to lamellipodia, where F-actin was high. In contrast, the distribution of cytosplasmic nonmuscle class II myosin was not altered. Expressions of myosin-1c and II were also demonstrated in B cells by Western blot. Although the inhibition of PLCgamma, PI3K and MEK-1 activation affected the spreading and dendrite formation in activated B cells, only PLCgamma and MEK-1 inhibition correlated with absence of myosin-1c polarization. Additionally, myosin-1c polarization was observed upon cross-linking of other surface molecules, suggesting a common mechanism for B cell spreading. This work shows that class I and class II myosin are expressed in B cells, are differentially distributed, and may participate in the morphological changes of these cells.

Actins↗
PubMed2003

Membrane fission: model for intermediate structures.

Membrane budding-fission is a fundamental process generating intracellular carriers of proteins. Earlier works were focused only on formation of coated buds connected to the initial membrane by narrow membrane necks. We present the theoretical analysis of the whole pathway of budding-fission, including the crucial stage where the membrane neck undergoes fission and the carrier separates from the donor membrane. We consider two successive intermediates of the reaction: 1), a constricted membrane neck coming out of aperture of the assembling protein coat, and 2), hemifission intermediate resulting from self-fusion of the inner monolayer of the neck, while its outer monolayer remains continuous. Transformation of the constricted neck into the hemifission intermediate is driven by the membrane stress produced in the neck by the protein coat. Although apparently similar to hemifusion, the fission is predicted to have an opposite dependence on the monolayer spontaneous curvature. Analysis of the further stages of the process demonstrates that in all practically important cases the hemifission intermediate decays spontaneously into two separate membranes, thereby completing the fission process. We formulate the "job description" for fission proteins by calculating the energy they have to deliver and the radii of the protein coat aperture which have to be reached to drive the fission process.

Cell Surface Extensions↗
PubMed2003

Requirement of autophosphorylated tyrosine 992 of EGF receptor and its docking protein phospholipase C gamma 1 for membrane ruffle formation.

Stimulation of the epidermal growth factor receptor (EGFR) produces membrane ruffles through the small G protein Rac1; however, the signaling pathway from EGFR to Rac1 has not yet been clarified. Here, we show that autophosphorylation of EGFR at tyrosine 992 is required for EGF-induced membrane ruffle formation in CHO cells. Signaling from the autophosphorylated tyrosine 992 appears to be mediated by phospholipase C (PLC) gamma 1. Furthermore, activation of Rac1 by EGF is inhibited by a PLC inhibitor. These results, taken together, suggest that autophosphorylation of EGFR at tyrosine 992 and the subsequent PLC gamma 1 activation transduce the signal to Rac1 to induce membrane ruffle formation.

Animals↗
PubMed2001

Plasticity and stabilization of neuromuscular and CNS synapses: interactions between thrombin protease signaling pathways and tissue transglutaminase.

The first association of the synapse as a potential site of neurodegenerative disease burden was suggested for Alzheimer's disease (AD) almost 30 years ago. Since then protease:protease inhibitor (P:PI) systems were first linked to functional regulation of synaptogenesis and synapse withdrawal at the neuromuscular junction (NMJ) more than 20 years ago. Confirmatory evidence for the involvement of the synapse, the rate-limiting or key unit in neural function, in AD did not become clear until the beginning of the 1990s. However, over the past 15 years evidence for participation of thrombin, related serine proteases and neural PIs, homologous and even identical to those of the plasma clot cascade, has been mounting. Throughout development a balance between stabilization forces, on the one hand, and breakdown influences, on the other, becomes established at synaptic junctions, just as it does in plasma clot proteins. The formation of protease-resistant cross-links by the transglutaminase (TGase) family of enzymes may add to the stability for this balance. The TGase family includes coagulation factor XIIIA and 8 other different genes, some of which may also influence the persistence of neural connections. Synaptic location of protease-activated, G-protein-coupled receptors (PARs) for thrombin and related proteases, their serpin and Kunitz-type PIs such as protease nexin I (PNI), alpha1-antichymotrypsin (alpha-ACT), and the Kunitz protease inhibitor (KPI)-containing secreted forms of beta-amyloid protein precursor (beta-APP), along with the TGases and their putative substrates, have all been amply documented. These findings strongly add to the conclusion that these molecules participate in the eventual structural stability of synaptic connections, as they do in coagulation cascades, and focus trophic activity on surviving terminals during periods of selective contact elimination. In disease states, this imbalance is likely to be shifted in favor of destabilizing forces: increased and/or altered protease activity, enhanced PAR influence, decreased and/or altered protease inhibitor function, reduction and/or alteration in tTG expression and activity, and alteration in its substrate profile. This imbalance further initiates a cascade of events leading to inappropriate programmed cell death and may well be considered evidence of synaptic apoptosis.

Amino Acid Sequence↗
PubMed2003

Regulation of cortical actin networks in cell migration.

The actin cytoskeleton is a primary determinant of cell shape and motility. Studies on actin regulatory proteins are now coupled with studies of the signal transduction that directs actin cytoskeleton reorganization, and we have gained insights into how external stimuli such as chemoattractants drive changes in actin cytoskeleton. Chemoattractants regulate actin regulatory proteins such as the Arp2/3 complex through WASP family proteins, ADF/cofilin downstream of LIM-kinase, and various other phosphoinositide-dependent or -independent pathways. Through branching of actin filaments, Arp2/3 complex-dependent actin polymerization is suffcient to generate the force necessary for protrusion.

Actin Depolymerizing Factors↗
PubMed2001

CED-12/ELMO, a novel member of the CrkII/Dock180/Rac pathway, is required for phagocytosis and cell migration.

The C. elegans genes ced-2, ced-5, and ced-10, and their mammalian homologs crkII, dock180, and rac1, mediate cytoskeletal rearrangements during phagocytosis of apoptotic cells and cell motility. Here, we describe an additional member of this signaling pathway, ced-12, and its mammalian homologs, elmo1 and elmo2. In C. elegans, CED-12 is required for engulfment of dying cells and for cell migrations. In mammalian cells, ELMO1 functionally cooperates with CrkII and Dock180 to promote phagocytosis and cell shape changes. CED-12/ELMO-1 binds directly to CED-5/Dock180; this evolutionarily conserved complex stimulates a Rac-GEF, leading to Rac1 activation and cytoskeletal rearrangements. These studies identify CED-12/ELMO as an upstream regulator of Rac1 that affects engulfment and cell migration from C. elegans to mammals.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Pulling back to move forward.

Animal cells can change shape and move by using actin polymerization to drive plasma membrane protrusion. Giannone and coworkers (this issue of Cell) describe how cells periodically pull back on these protrusions in order to sense and respond to the rigidity of their environment.

Actins↗
PubMed2003

Effect of spark plasma sintering on the microstructure and in vitro behavior of plasma sprayed HA coatings.

The crystalline phases and degree of crystallinity in plasma sprayed calcium phosphate coatings on Ti substrates are crucial factors that influence the biological interactions of the materials in vivo. In this study, plasma sprayed hydroxyapatite (HA) coatings underwent post-spray treatment by the spark plasma sintering (SPS) technique at 500 degrees C, 600 degrees C, and 700 degrees C for duration of 5 and 30 min. The activity of the HA coatings before and after SPS are evaluated in vitro in a simulated body fluid. The surface microstructure, crystallinity, and phase composition of each coating is characterized by scanning electron microscopy and X-ray diffractometry before, and after in vitro incubation. Results show that the plasma sprayed coatings treated for 5 min in SPS demonstrated increased proportion of beta-TCP phase with a preferred-orientation in the (214) plane, and the content of beta-TCP phase corresponded to SPS temperature, up to 700 degrees C. SPS treatment at 700 degrees C for 30 min enhanced the HA content in the plasma spray coating as well. The HA coatings treated in SPS for 5 min revealed rapid surface morphological changes during in vitro incubation (up to 12 days), indicating that the surface activity is enhanced by the SPS treatment. The thickest apatite layer was found in the coating treated by SPS at 700 degrees C for 5 min.

Biomimetic Materials↗
PubMed2003

New biomorphic SiC ceramics coated with bioactive glass for biomedical applications.

A new generation of light, tough and high-strength material for medical implants for bone substitutions with a good biological response is presented. The innovative product that fulfills all these requirements is based on biomorphic silicon carbide ceramics coated with a bioactive glass layer. The combination of the excellent mechanical properties and low density of the biomorphic SiC ceramics, used as a base material for implants, with the osteoconducting properties of the bioactive glass materials opens new possibilities for the development of alternative dental and orthopedic implants with enhanced mechanical and biochemical properties that ensures optimum fixation to living tissue. Biomorphic SiC is fabricated by molten-Si infiltration of carbon templates obtained by controlled pyrolysis of wood. Through this process, the microstructure of the final SiC product mimics that of the starting wood, which has been perfected by natural evolution. The basic features of such microstructure are its porosity (ranging from 30% to 70%) and its anisotropy, which resembles the cellular microstructure and the mechanical characteristics of the bone. The SiC ceramics have been successfully coated with a uniform and adherent bioactive glass film by pulsed laser ablation using an excimer ArF laser. The excellent coverage of the SiC rough surface without film spallation or detachment is demonstrated. In order to assess the coating bioactivity, in vitro tests by soaking the samples in simulated body fluid have been carried out. After 72 h, the formation of a dense apatite layer has been observed even in interconnecting pores by SEM and energy dispersive X-ray spectroscopy analysis demonstrating the bioactive response of this product.

Biomedical Engineering↗
PubMed2003

Corpus callosum and visual cortex of mice with deletion of the NMDA-NR1 receptor: I. Accelerated development of callosal projection neurons.

Many pharmacological experiments show that the ionotropic receptor NMDA has both neurotrophic and neuroexcitotoxic effects. The neurotrophic function is manifested in many ways including acceleration of neuronal development, enhancement of neuronal migration, neuroprotection, blockage of apoptosis, prevention of aging and prematurity, as well as effects on synaptic plasticity and synaptogenesis. On the other hand, the neuroexcitotoxic function is manifested in its role in neurological and psychiatric diseases such as epilepsy, Parkinson's disease and schizophrenia. The present study explores the consequences of complete and partial absence of NMDA-NR1 receptors throughout development. Using DiI tracing in vitro, the development of corpus callosum projection neurons in transgenic mice with deletion of the NMDA-NR1 receptor was observed in visual cortex. Compared to littermate controls, the histogenesis and neuronal development of corpus callosum cells of origin was found to be accelerated in NR1-/- mice. That is, the corpus callosum projection neurons in NR1 knockout mice developed earlier and faster than in littermate heterozygous and wild-type mice. However, the corpus callosum projection neurons in NR1 heterozygous mice developed earlier and faster than in littermate wild-type mice. This suggests that NMDA-NR1 receptors are involved in sequencing and/or temporal regulation of neuronal development, and that there is a gene-dose effect. Studies from other laboratories suggest that the observed phenomenon of prematurity or accelerated development is a direct effect of altered expression of genes found in mice with deletion of the NMDA-NR1 receptor.

Animals↗
PubMed2002

Molecular morphogens for dendritic spines.

Three protein components of the postsynaptic density--Shank, Homer and SPAR--have been found to regulate the structural and molecular organization of dendritic spines. These new studies reveal linkages between receptor complexes, the actin cytoskeleton and signaling molecules that help shape spines.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Orexin actions in hypothalamic paraventricular nucleus: physiological consequences and cellular correlates.

Orexinergic neurons originating in the perifornical, lateral hypothalamus project to numerous brain sites including neuroendocrine centers known to be important in the physiologic response to stress. Those projections suggest an action of endogenous orexin on adrenocorticotropin (ACTH) release, either by neuromodulatory effects in the paraventricular nucleus (PVN), or by neuroendocrine actions in the pituitary gland following release into the median eminence. We sought to determine if exogenously applied orexin A might act in the brain to alter ACTH release and to determine if a site of action in the hypothalamic paraventricular nucleus could be identified. Cerebroventricular administration of orexin A in conscious male rats resulted in a dose-related elevation in circulating ACTH levels. At 30 min post-infusion, ACTH levels were elevated 2.5-fold by the low dose of orexin A (0.3 nmol), 5.7-fold by the middle dose tested (1.0 nmol), and 7.5-fold by the highest dose tested (3.0 nmol). Pretreatment with a CRH-antagonist (i.v.) blocked the ability of i.c.v. administered orexin A to activate the hypothalamo-pituitary-adrenal (HPA) axis. Bath application of orexin A in hypothalamic slice preparations resulted in depolarizations (8.0+/-0.6 mV), accompanied by increases in spike frequency in identified magno- and parvocellular neurons in the PVN. Our data suggest a potential role for endogenous orexin in the hypothalamic regulation of stress hormone secretion.

Adrenocorticotropic Hormone↗
PubMed2003

Activity-dependent remodeling of presynaptic inputs by postsynaptic expression of activated CaMKII.

Competitive synaptic remodeling is an important feature of developmental plasticity, but the molecular mechanisms remain largely unknown. Calcium/calmodulin-dependent protein kinase II (CaMKII) can induce postsynaptic changes in synaptic strength. We show that postsynaptic CaMKII also generates structural synaptic rearrangements between cultured cortical neurons. Postsynaptic expression of activated CaMKII (T286D) increased the strength of transmission between pairs of pyramidal neuron by a factor of 4, through a modest increase in quantal amplitude and a larger increase in the number of synaptic contacts. Concurrently, T286D reduced overall excitatory synaptic density and increased the proportion of unconnected pairs. This suggests that connectivity from some synaptic partners was increased while other partners were eliminated. The enhancement of connectivity required activity and NMDA receptor activation, while the elimination did not. These data suggest that postsynaptic activation of CaMKII induces a structural remodeling of presynaptic inputs that favors the retention of active presynaptic partners.

Alanine↗
PubMed2000

BMP, Wnt and Hedgehog signals: how far can they go?

Wnt, Hedgehog and bone morphogenetic proteins function as either short-range or long-range signaling molecules depending on the tissue in which they are expressed. In the past year, filapodia-like cytoplasmic extensions, cell-surface proteogylcans and/or extracellular binding proteins have been identified that may enable these molecules to signal at a distance. Furthermore, recent studies suggest that variations in the signaling range of these molecules may be due to tissue-specific differences in intracellular processing or tissue-restricted expression of binding proteins.

Animals↗
PubMed2003

Cell-fate specification in the epidermis: a common patterning mechanism in the root and shoot.

The specification of epidermal hairs in Arabidopsis provides a useful model for the study of pattern formation in plants. Although the distributions of hair cells in the root and shoot appear quite different, recent studies show that pattern formation in each relies on a common cassette of transcriptional regulators. During development in each organ, neighboring cells compete to express regulators that specify the primary cell fate (including WEREWOLF [WER]/GLABRA1 [GL1], GL3/bHLH, TRANSPARENT TESTA GLABRA [TTG], and GL2), as well as those that prevent their neighbors from adopting this fate (including CAPRICE [CPC] and TRIPTYCHON [TRY]). The basic mechanism of lateral inhibition with feedback that has been uncovered by recent studies provides a conceptual framework for understanding how patterns of cell fate in general may be specified during plant development.

Arabidopsis↗
PubMed2001

C. elegans CED-12 acts in the conserved crkII/DOCK180/Rac pathway to control cell migration and cell corpse engulfment.

We have identified and characterized a novel C. elegans gene, ced-12, that functions in the conserved GTPase signaling pathway mediated by CED-2/Crkll, CED-5/DOCK180, and CED-10/Rac to control cell migration and phagocytosis of apoptotic cells. We provide evidence that ced-12 likely acts upstream of ced-10 during cell migration and phagocytosis and that CED-12 physically interacts with CED-5 and forms a ternary complex with CED-2 in vitro. We propose that the formation and localization of a CED-2-CED-5-CED-12 ternary complex to the plasma membrane activates CED-10, leading to the cytoskeletal reorganization that occurs in the polarized extension of cell surfaces in engulfing cells and migrating cells. We suggest that CED-12 counterparts in higher organisms regulate cytoskeleton dynamics, as CED-12 does in C. elegans.

Amino Acid Sequence↗