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Results for “Chain Migration”

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PubMed2002

Hb Molfetta [beta126(H4)Val-->Leu, GTG-->CTG]: a new, silent, neutral beta chain variant found in an Italian woman.

We have identified a new neutral hemoglobin variant in a pregnant Italian woman, that resulted from a GTG-->CTG replacement at codon 126 of the beta chain, corresponding to a Val-->Leu amino acid change at position beta126(H4). Thermal and isopropanol stability tests were normal and there were no abnormal clinical features. Routine electrophoretic and ion exchange chromatographic methods for hemoglobin separation failed to show this variant, but reversed phase high performance liquid chromatography revealed an abnormal peak eluting near the normal beta chain. No abnormal tryptic peptide was revealed on the high performance liquid chromatographic elution pattern of the total globin digest. The mutation was determined at the DNA level by amplification of the three beta exons by polymerase chain reaction and direct sequencing of one exon that showed an abnormal migration on single strand conformational polymorphism analysis.

Adult↗

PubMed2000

Development of an ultralow-light-level luminescence image analysis system for dynamic measurements of transcriptional activity in living and migrating cells.

We have developed an approach to study in single living epithelial cells both cell migration and transcriptional activation, which was evidenced by the detection of luminescence emission from cells transfected with luciferase reporter vectors. The image acquisition chain consists of an epifluorescence inverted microscope, connected to an ultralow-light-level photon-counting camera and an image-acquisition card associated to specialized image analysis software running on a PC computer. Using a simple method based on a thin calibrated light source, the image acquisition chain has been optimized following comparisons of the performance of microscopy objectives and photon-counting cameras designed to observe luminescence. This setup allows us to measure by image analysis the luminescent light emitted by individual cells stably expressing a luciferase reporter vector. The sensitivity of the camera was adjusted to a high value, which required the use of a segmentation algorithm to eliminate the background noise. Following mathematical morphology treatments, kinetic changes of luminescent sources were analyzed and then correlated with the distance and speed of migration. Our results highlight the usefulness of our image acquisition chain and mathematical morphology software to quantify the kinetics of luminescence changes in migrating cells.

Animals↗

PubMed1994

Neutrophil migration inhibitory properties of polyunsaturated fatty acids. The role of fatty acid structure, metabolism, and possible second messenger systems.

The n-3 polyunsaturated fatty acids (PUFA) appear to have antiinflammatory properties that can be partly explained by their biological activity on leukocytes. Since leukocyte emigration is an essential component of the inflammatory response, we have examined the effects of the n-3 PUFA (eicosapentaenoic and docosahexaenoic acids) on neutrophil random and chemotactic movement. Preexposure of neutrophils for 15-30 min to 1-10 micrograms/ml PUFA reduced the random and chemotactic migration to both FMLP- and fungi-activated complement. The inhibitory effect diminished with increasing saturation and carbon chain length, and methylation abolished this activity. Arachidonic and docosahexaenoic acids were the most active fatty acids. The PUFA concentration required to inhibit migration was dependent on cell number, suggesting that the fatty acid effects on leukocyte migration in vivo may be governed by the stage of the inflammatory response. It was concluded that the PUFA rather than their metabolites were responsible for the inhibition since: (a) antioxidants did not prevent the PUFA-induced migration inhibition and the hydroxylated intermediates were less active, and (b) inhibitors of the cyclooxygenase and lipoxygenase pathways were without effect. Inhibitors of protein kinases and calmodulin-dependent enzyme system did not prevent the PUFA-induced migration inhibition, which was also independent of phospholipase D-catalyzed hydrolysis of phospholipids. It is also shown that PUFA decrease the FMLP-induced Ca2+ mobilization.

Calcium↗

PubMed1985

The in vitro activity of lectin I from mistletoe (ML I) and its isolated A and B chains on functions of macrophages and polymorphonuclear cells.

We investigated the effects of ML I and its isolated chains, A and B, in regard to selected functions of phagocytes (human granulocytes, paraffin-oil stimulated M phi from guinea pigs). On these cells, ML I has no cytotoxic effect between 10(-14) and 10(-8) (trypan blue exclusion and ethidium bromide exclusion). Over the same concentration range, ML I and B chain diminish the negative surface charge of M phi and agglutinate M phi at concentrations greater than or equal to 2 X 10(-8) M (ML I) and greater than or equal to 3 X 10(-7) M (B chain), respectively. The diminishing of the negative surface charge shows two peaks, indicating the existence of two types of receptors on the M phi surface with different affinities for sugar-binding sites. Moreover, the B chain shows a third peak at higher concentrations (3 X 10(-8) M) that could be inhibited by D-galactose (greater than or equal to 10(-4) M). In comparison, the A chain reduces the surface charge at concentrations over 3 X 10(-7) M, but D-galactose has no effect on this. By means of the agarose droplet test, the spontaneous migration of M phi is inhibited in the sequence ML I much greater than B chain greater than A chain. The phagocytic activity of human leukocytes tested with a radiometric phagocytosis technique reveals an increasing effect only for the B chain; ML I and the A chain have no effect. Perhaps the mechanism of the described activities of ML I and its B chain are comparable with the action of lymphokines activating M phi.

Animals↗

PubMed2001

Recruitment of a myosin heavy chain kinase to actin-rich protrusions in Dictyostelium.

Nonmuscle myosin II plays fundamental roles in cell body translocation during migration and is typically depleted or absent from actin-based cell protrusions such as lamellipodia, but the mechanisms preventing myosin II assembly in such structures have not been identified [1-3]. In Dictyostelium discoideum, myosin II filament assembly is controlled primarily through myosin heavy chain (MHC) phosphorylation. The phosphorylation of sites in the myosin tail domain by myosin heavy chain kinase A (MHCK A) drives the disassembly of myosin II filaments in vitro and in vivo [4]. To better understand the cellular regulation of MHCK A activity, and thus the regulation of myosin II filament assembly, we studied the in vivo localization of native and green fluorescent protein (GFP)-tagged MHCK A. MHCK A redistributes from the cytosol to the cell cortex in response to stimulation of Dictyostelium cells with chemoattractant in an F-actin-dependent manner. During chemotaxis, random migration, and phagocytic/endocytic events, MHCK A is recruited preferentially to actin-rich leading-edge extensions. Given the ability of MHCK A to disassemble myosin II filaments, this localization may represent a fundamental mechanism for disassembling myosin II filaments and preventing localized filament assembly at sites of actin-based protrusion.

Actins↗

PubMed2002

Hematopoietic stem cells are uniquely selective in their migratory response to chemokines.

Although hematopoietic stem cell (HSC) migration into and out of sites of active hematopoiesis is poorly understood, it is a critical process that underlies modern clinical stem cell transplantation and may be important for normal hematopoietic homeostasis. Given the established roles of chemotactic cytokine (chemokine)-directed migration of other leukocyte subsets, the migration of murine HSC to a large panel of CC and CXC chemokines was investigated. HSC migrated only in response to stromal derived factor-1alpha, the ligand for the CXC chemokine receptor 4 (CXCR4). CXCR4 expression by HSC was confirmed by reverse transcription polymerase chain reaction analysis. Surprisingly, HSC also expressed mRNA for CCR3 and CCR9, although they failed to migrate to the ligands for these receptors. The sharply restricted chemotactic responsiveness of HSC is unique among leukocytes and may be necessary for the specific homing of circulating HSC to bone marrow, as well as for the maintenance of HSC in hematopoietic microenvironments.

Animals↗

PubMed1993

Cloning and functional expression of a cDNA encoding the catalytic subunit of bovine enterokinase.

Enterokinase (enteropeptidase) is a heterodimeric serine protease that is responsible for the physiological activation of trypsinogen by highly specific cleavage of the trypsinogen activation peptide following the sequence (Asp)4-Lys. In this paper, we report the cloning and functional expression of a cDNA encoding the catalytic domain (light chain) of bovine enterokinase. The nucleotide sequence of this cloned cDNA predicts a 235-amino acid polypeptide that shares a high degree of homology with a variety of mammalian serine proteases involved in digestion, coagulation, and fibrinolysis. We have developed a novel expression method for the enzyme which utilizes the secretory leader and propeptide of the mammalian serine protease PACE fused to the enterokinase light chain amino terminus. Efficient cleavage of the paired dibasic amino acid cleaving enzyme (PACE) propeptide was achieved by coexpression with human PACE or yeast KEX2. The mature product migrates at 43,000 Da on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, comparable to light chain derived from bovine duodena, and exhibited high levels of activity in cleaving the enterokinase-specific fluorogenic substrate Gly-(Asp)4-Lys-beta-naphthylamide. The recombinant single-chain form of enterokinase was also capable of activating trypsinogen, indicating that the specificity of the enzyme for its natural substrate is retained even in the absence of the noncatalytic enterokinase heavy chain.

Amino Acid Sequence↗

PubMed1999

Widening of the elution window in micellar electrokinetic chromatography with cationic surfactants. II. Cationic additives and modifiers of the electroosmotic flow.

In micellar electrokinetic chromatography (MEKC) with cationic surfactants the migration window is significantly narrower than with anionic surfactants. In order to overcome this disadvantage of cationic surfactants, it is investigated whether it is possible to widen the migration window by reducing the velocity of the aqueous phase while the electrophoretic mobility of the micelles is maintained. Short chain alkylammonium compounds, hexamethonium bromide and hydroxypropylmethylcellulose are tested as additives to the separation electrolyte with the potential to improve the migration window via reducing the velocity of the electroosmotic flow. It will be shown that these modifiers can be successfully used in order to widen the migration window in MEKC with cationic surfactant employing an alkyltrimethylammonium bromide as micelle forming agents. Influence of the modifiers selected on retention of neutral and acidic solutes and on efficiency of the separation system is investigated.

Cations↗

PubMed2003

Heparan sulfate proteoglycans modulate monocyte migration across cerebral endothelium.

Heparan sulfate proteoglycans (HSPGs) are known to participate in a wide range of biological events, including cellular trafficking. In this study we report that in situ cerebral blood vessels highly express HSPGs. Of the syndecan family, syndecan-2 is highly expressed on virtually all brain vessels and syndecan-1 and -3 are only present on larger blood vessels. These endothelial HSPGs have a functional role in monocyte diapedesis across brain endothelium, as assessed in our in vitro adhesion and migration assays. Our data indicate that heparin prevents monocyte adhesion to brain endothelium by interacting solely with the monocyte. Transendothelial migration of monocytes can be prevented by preincubation of brain endothelium with heparin by enzymatic removal of heparan sulphate side chains or by inhibition of cellular sulfation. Blocking of G-protein-dependent signaling in the monocytes prevented monocyte adhesion and migration to similar extent, suggesting that G-dependent signaling may be involved in HSPG-mediated monocyte adhesion and transendothelial migration. Our data demonstrate that brain endothelial HSPGs have a modulatory role in the transendothelial migration of monocytes in a direct and indirect fashion and may therefore contribute to the formation of neuroinflammatory lesions.

Animals↗

PubMed2000

The effect of antigen stimulation on alpha(4), beta(1) and beta(7) chain integrin expression and function in CD4+ cells.

BACKGROUND: The alpha(4) integrin, as alpha(4)beta(1) (VLA-4) or alpha(4)beta(7), is critical for T cell migration and proliferation, although its functional modulation remains poorly understood. We hypothesized that increased receptor density, based on new receptor chain synthesis, was one such mechanism. We examined the surface receptor density of the alpha(4) and beta(1) chains on CD4+CD45RO+ cells, and the mRNA expression of these and the beta(7) chain in response to allergen and nonallergen antigen stimulation. METHODS: Flow-cytometric analyses for CD49d, CD29, and CD45RO were performed on T cell lines specific for timothy, tetanus, and Candida from atopic and nonatopic donors. RNA was extracted from cells sorted to select CD4+/CD49d-positive cells before and after stimulation. Equivalent amounts of cDNA for beta-actin, alpha(4), beta(1) and beta(7) were used in PCR, and the products were quantified using phosphoimaging. RESULTS: CD49d expression is heterogeneous on T cell lines and is upregulated by antigen stimulation on CD4+ T cells. The surface expression on CD4+CD45RO+ timothy allergen or tetanus toxoid T cell lines is at least double that found on CD45RO- cells. Antigen stimulation upregulated CD49d expression on the CD4+CD45RO+ subpopulation of both cell lines although it was not as significant as in the case of all CD4+ T cells. CD29 surface expression behaves similarly. Candida had no effect on CD49d or CD29. Messenger RNA expression for the alpha(4) chain (CD49d) is significantly upregulated 48 h following the addition of timothy or tetanus. beta(7) chain expression also rises significantly on both cell lines. beta(1) chain expression increases, but not significantly. CONCLUSIONS: The surface expression of the CD49d is heterogeneous and much higher on CD4+CD45RO+ cells than on CD4+RO- T cells. The CD49d integrin chain on CD4+ T cells is upregulated following antigen exposure. However, the CD4+CD45RO+ subpopulation is only partially responsible for this increase suggesting other T cells to have this receptor expression upregulated. CD29 expression behaves similarly. Messenger RNA expression increases coordinately for alpha(4), beta(7), and not significantly for beta(1) in these cells. These observations provide a potential mechanism for the selective accumulation of T cells at sites of inflammation, and suggest an important point of intervention for allergic and inflammatory disease.

Allergens↗

PubMed1983

Botulinum neurotoxin type E: studies on mechanism of action and on structure-activity relationships.

Single chain type E botulinum neurotoxin was isolated from culture fluids of Clostridium botulinum (strain Alaska E-43). The neurotoxin, which migrated as a single band in polyacrylamide gel electrophoresis with sodium dodecylsulfate, had a molecular weight of approximately 147,000. Single chain type E neurotoxin that was exposed to trypsin was converted to a dichain molecule. Pretreatment of the single chain molecule with 1,2-cyclohexanedione, a reagent that selectively modifies arginine residues, inhibited trypsin-induced generation of the dichain molecule. In dose-response experiments (10(-13) to 10(-9) M) on the isolated neuromuscular junction (phrenic nerve-hemidiaphragm preparation), the dichain neurotoxin was approximately two orders of magnitude more potent than the single chain neurotoxin. Neither specie of neurotoxin (1 pmol/mouse, in vivo; 1 X 10(-11) M, in vitro) was very effective in blocking autonomic transmission (vagus nerve-atrium preparation). The neuromuscular blocking action of the dichain molecule was divided into a sequence of three steps. There was an initial binding step that was relatively rapid, little influenced by temperature and which left the neurotoxin partially accessible to the neutralizing effects of antitoxin. There was a translocation step that was temperature dependent, antagonized by ammonium chloride and methylamine hydrochloride and which caused the neurotoxin to become inaccessible to the neutralizing effects of antitoxin. Finally, there was an intracellular lytic step, during which the toxin blocked excitation-secretion coupling.

Animals↗

PubMed1994

Tetanus toxin light chain cleaves a vesicle-associated membrane protein (VAMP) isoform 2 in rat pancreatic zymogen granules and inhibits enzyme secretion.

Pancreatic acinar cells, a model cell type for the study of exocytosis in non-excitable cells, were used here to test the hypothesis that molecular mechanisms regulating exocytosis from neuronal and neuroendocrine cells may also be utilized in exocrine cells. Using specific antisera raised against vesicle-associated membrane protein (VAMP) isoforms 1 and 2, we have identified VAMP-2, but not VAMP-1, immunoreactive proteins on rat pancreatic acinar cell secretory (zymogen) granules. This 18-kDa protein co-migrated with rat brain synaptic vesicle VAMP-2. Tetanus toxin (TeTx) light chain caused complete cleavage of this protein, which was prevented by the addition of EDTA. This toxin also inhibited in a dose-dependent manner Ca(2+)-stimulated enzyme secretion by up to approximately 30% in streptolysin O-permeabilized acini. This effect of TeTx on secretion was prevented by the zinc endopeptidase inhibitor captopril or by boiling the toxin. Incomplete inhibition of secretion by TeTx may suggest that TeTx-insensitive or VAMP-2-independent mechanisms also regulate exocytosis. In support, TeTx light chain was without effect on Rab3AL (effector domain peptide of Rab3)-mediated potentiation of Ca(2+)-stimulated secretion. These results indicate that a TeTx-sensitive VAMP-2-like protein on zymogen granules participates in Ca(2+)-regulated pancreatic enzyme secretion and that undefined Rab3AL-activated mechanisms may act independently to regulate exocytosis.

Amino Acid Sequence↗

PubMed2003

Migration of lubricants from food packagings. Screening for lipid classes and quantitative estimation using normal-phase liquid chromatographic separation with evaporative light scattering detection.

A normal-phase high-performance liquid chromatography (NP-HPLC) method is introduced for the identification and quantitative estimation of 12 lipid classes (paraffin, wax esters, cholesterol esters, fatty acid methyl esters, triacyl glycerols, fatty alcohols, free fatty acids, cholesterol, 1,3-diacyl glycerols, 1,2-diacyl glycerols, monoacyl glycerols and fatty acid amide) used as lubricantsin food packaging materials. The HPLC separation is carried out on a LiChrospher Diol (100 A, 5 microm, 125 mm x 3 mm) column with gradient elution (isooctane/0.1% acetic acid in tert-butyl methyl ether) and evaporative light scattering detection (ELSD). The method has been calibrated with representatives of each class in working ranges of about 5-150 mg/l, depending on the lipid class. Intra-day variance for all representatives range from 1.9 to 5.1%, inter-day variances from 7.0 to 26.5% and the limits of detection from 0.79 to 3.65 mg/l (except for two classes). A simple sample preparation could be established for the determination of migrating lubricants obtained from packaging materials containing external or internal lubricants. Since the detector response depends on the chain length and the degree of saturation, the quantification of a lipid class with unknown composition is only semi-quantitative. The amount of migrating lubricants from an epoxy-based can coating could be estimated with 0.3 mg/dm2 and from a light weight container with 5.5 mg/dm2.

Chromatography, High Pressure Liquid↗

PubMed1994

Phenotypic characterization of CD4-/alpha beta TCR+ and gamma delta TCR+ T cells with a transendothelial migratory capacity.

During inflammation, both CD4+ and CD4- T lymphocytes extravasate into perivascular tissues by adhering to and migrating through the vascular endothelium. These studies were undertaken to characterize the phenotype of CD4- T cells that have a capacity to migrate through endothelium. Results show that CD4- T cells exhibit a greater capacity to migrate through endothelial cells (EC) than CD4+ T cells; and that TCR-gamma delta+ T cells exhibited the greatest migratory capacity. The migrating CD8+ T cell population was enriched in CD45RO+/L-selectin-/LFA-1bright/CD29bright/CD 44bright cells. TNF-alpha-activated EC did not support increased CD4- T cell transendothelial migration and changes in the phenotype of the migrating CD8+ T cells. The migrating CD4- T cell population was enriched in VLA-2+ T cells and expressed increased densities of VLA-4, VLA-5, and VLA-6. The migrating TCR-gamma delta+ T cell population contained both CD8dim and CD8- T cells. Moreover, the migrating gamma delta T cell population was not different from the initial or nonadherent population in that it contained CD45RO+, CD45RA+, and L-selectin+ cells. Finally, migrating TCR-gamma delta+ T cells contained cells expressing V delta 2 and V gamma 9 TCR chains, but these were not enriched compared with the initial population. These studies have characterized the CD4- T cells that are capable of transendothelial migration in vitro. The results are consistent with the conclusion that unique subpopulations of CD8+ alpha beta and CD8+ and CD8- gamma delta T cells gain access to inflammatory sites by virtue of their intrinsic ability to migrate across the endothelium.

CD4 Antigens↗

PubMed2005

Focal adhesion kinase signaling regulates cardiogenesis of embryonic stem cells.

The signaling steps that induce cardiac differentiation in embryonic stem (ES) cells are incompletely understood. We examined the effect of adhesion signaling including Src and focal adhesion kinase (FAK) on cardiogenesis in mouse ES cells using alpha-myosin heavy chain promoter-driven enhanced green fluorescent protein or luciferase as reporters. Cardiac transcription factors including Nkx2.5 and Tbx5 mRNA were first expressed at day 4 in hanging drop embryoid bodies, and adhesion of embryoid bodies to surfaces at or before that day strongly inhibited differentiation of ES cells to cardiomyocytes. Since adhesion signaling could suppress cardiogenesis through Src kinases, embryoid bodies were exposed to the small molecule PP2, known as a Src family kinase inhibitor. PP2 during embryoid body adhesion dramatically increased cardiomyocyte differentiation and decreased mRNA expression of neuronal cellular adhesion molecule and alpha-fetoprotein, neuroectodermal, and endodermal markers, respectively. Surprisingly, although there was an interaction between Src and FAK in cardiogenesis, the procardiogenic effect of PP2 appeared incompletely explained by Src kinase inhibition, since another Src family kinase inhibitor, SU6656, failed to induce cardiogenesis. Instead, PP2 specifically inhibited adhesion-induced FAK phosphorylation. In ES cells stably expressing FAK-related nonkinase, which functions as a dominant negative FAK, cell migration from embryoid bodies was inhibited, whereas alpha-myosin heavy chain expression and myosin-stained cardiomyocytes were increased, suggesting that reducing cell motility may contribute to cardiogenesis. These data indicate that FAK is a key regulator of cardiogenesis in mouse ES cells and that FAK signaling within embryoid bodies can direct stem cell lineage commitment.

Animals↗

PubMed2002

Laminin 10/11: an alternative adhesive ligand for epidermal keratinocytes with a functional role in promoting proliferation and migration.

We have investigated the expression and function of the isoforms of laminin bearing the alpha5 chain, i.e. laminin-10/11 in neonatal and adult human skin. By immunostaining human skin derived from a variety of anatomic sites, we found that the laminin-alpha5 chain is expressed abundantly in the basement membrane underlying the interfollicular epidermis and the blood vessels in the dermis. Interestingly, while the expression level of the well-studied laminin-5 isoform did not change significantly with age, laminin-10/11 (alpha5 chain) appeared to decrease in the basement membrane underlying the epidermis, in adult skin. In contrast, the levels of laminin-10/11 in the basement membrane underlying blood vessels remained unchanged in neonatal vs. adult skin. Importantly, in vitro cell adhesion assays demonstrated that laminin-10/11 is a potent adhesive substrate for both neonatal and adult keratinocytes and that this adhesion is mediated by the alpha3beta1 and alpha6beta4 integrins. Adhesion assays performed with fractionated basal keratinocytes showed that stem cells, transit amplifying cells and early differentiating cells all adhere to purified laminin-10/11 via these receptors. Further, laminin-10/11 provided a proliferative signal for neonatal foreskin keratinocytes, adult breast skin keratinocytes, and even a human papillomavirus type-18 transformed tumorigenic keratinocyte cell line in vitro. Finally, laminin-10/11 was shown to stimulate keratinocyte migration in an in vitro wound healing assay. These results provide strong evidence for a functional role for laminin-10/11 in epidermal proliferation during homeostasis, wound healing and neoplasia.

Adult↗

PubMed2000

Extracellular-regulated kinase activation and CAS/Crk coupling regulate cell migration and suppress apoptosis during invasion of the extracellular matrix.

Regulation of cell migration/invasion is important for embryonic development, immune function, and angiogenesis. However, migratory cells must also coordinately activate survival mechanisms to invade the extracellular matrix and colonize foreign sites in the body. Although invasive cells activate protective programs to survive under diverse and sometimes hostile conditions, the molecular signals that regulate these processes are poorly understood. Evidence is provided that signals that induce cell invasion also promote cell survival by suppressing apoptosis of migratory cells. Extracellular-regulated kinase (ERK) activation and molecular coupling of the adaptor proteins p130 Crk-associated substrate (CAS) and c-CrkII (Crk) represent two distinct pathways that induce cell invasion and protect cells from apoptosis in a three-dimensional collagen matrix. CAS/Crk-mediated cell invasion and survival requires activation of the small GTPase Rac, whereas ERK-induced cell invasion, but not survival requires myosin light chain kinase activation and myosin light chain phosphorylation. Uncoupling CAS from Crk or inhibition of ERK activity prevents migration and induces apoptosis of invasive cells. These findings provide molecular evidence that during invasion of the extracellular matrix, cells coordinately regulate migration and survival mechanisms through ERK activation and CAS/Crk coupling.

Animals↗

PubMed1990

The coalescent and the genealogical process in geographically structured population.

We shall extend Kingman's coalescent to the geographically structured population model with migration among colonies. It is described by a continuous-time Markov chain, which is proved to be a dual process of the diffusion process of stepping-stone model. We shall derive a system of equations for the spatial distribution of a common ancestor of sampled genes from colonies and the mean time to getting to one common ancestor. These equations are solved in three particular models; a two-population model, the island model and the one-dimensional stepping-stone model with symmetric nearest-neighbour migration.

Genetics, Population↗