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PubMed1994

Screening for cytokine messenger ribonucleic acids in purified human decidual lymphocyte populations by the reverse-transcriptase polymerase chain reaction.

At the time of human embryo implantation, large numbers of maternal CD56brightCD16- NK cells appear in the uterus. These unusual lymphocytes are believed to control the migration and differentiation of highly invasive fetally derived trophoblast cells, which infiltrate into the maternal uterus to remodel the spiral arteries during the first trimester. One possible mechanism of control is by cytokine production. In this study, highly purified (> 99%) populations of first trimester decidual CD56brightCD16- NK cells and CD3+ T lymphocytes were obtained by using a FACS. These cells were examined by reverse transcriptase PCR for their expression of mRNAs for the following cytokines: granulocyte-macrophage (GM)-CSF, CSF-1, TNF-alpha, IFN-gamma, TGF-beta 1, leukemia-inhibitory factor (LIF), and IL-2. Then, the expression was compared with that of resting PBL. The identity of the PCR products was verified by Southern blotting and hybridization with cytokine-specific probes. Both decidual CD56brightCD16- NK cells and CD3+ T cells were found to express mRNA for CSF-1, TNF-alpha, IFN-gamma TGF-beta 1, and LIF, but GM-CSF mRNA was detected only in CD56bright NK cells. IL-2 mRNA was detected in only some decidual T cell samples, and then only after at least two rounds of amplification. In contrast, peripheral blood CD56brightCD16- NK cells, CD56dimCD16+ NK cells, and CD3+ T cells expressed mRNA only for TNF-alpha and TGF-beta 1, but not for GM-CSF, CSF-1, IFN-gamma, LIF, or IL-2. These results suggest that both decidual NK cells and decidual T cells produce a variety of cytokines that may be involved in the control of trophoblast migration and differentiation during pregnancy.

Antigens, CD↗

PubMedDate not supplied

Lack of effect of extremely low frequency electromagnetic fields on cyclin-dependent kinase 4 inhibitor gene p18(INK4C) in electric energy workers.

BACKGROUND: Long-term exposure to extremely low frequency magnetic fields (ELF-MFs) may be a risk factor for human cancer. One mechanism through which ELF-MFs could influence neoplastic development is the deletion/mutation of cancer-related genes. Cellular proliferation follows an orderly progression through the cell cycle, which is governed by different cyclins and cyclin-dependent kinase inhibitors (CDKIs). The putative tumor suppressor gene p18(INK4C) encodes a specific inhibitor of cyclin D-cyclin-dependent kinase 4 inhibitor complexes having an important role in cell-cyclin regulation. It has been found to be deleted/mutated in a variety of human cancers. Therefore, this study is to investigate whether or not long-term extremely low frequency electromagnetic field exposure may be a risk factor for human cancer due to the gene p18(INK4C) deletion/mutation. METHODS: The study was carried out on 31 male electric workers and 30 healthy males between 30 and 40 years of age from the same geographic area and with similar lifestyles. We studied both groups by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP). RESULTS: In comparison to the controls, band migration of exon 1 was found to be indifferent in all the subjects tested. However, only exon 2 of two electric workers was slow in migration with respect to both control and other subjects in the same class. This slow migration suggests that point mutations or polymorphisms may exist in this region of the p18(INK4C) gene. The relative risk (RR) for the unmatched analysis was 1,069 (95% confidence interval [CI] 0.975-1.172). CONCLUSIONS: The results suggest that long-term ELF-MFs exposure does not significantly increase the risk of cancer.

Adult↗

PubMed1978

Mediation of cytotoxic functions by classes and subclasses of sheep antibody reactive with cell surface immunoglobulin idiotypic and constant region determinants.

Sheep antibodies, reactive with either the idiotypic or constant region antigenic determinants of the immunoglobulin light chain on guinea-pig L2C leukaemic cells, were separated into IgM and into the two subclasses of IgG, IgG1 and IgG2. Antibody of both IgG subclasses inhibited the migration of L2C cells along plastic surfaces; IgM was only weakly inhibitory. Antibody of class IgM and of subclass IgG1 mediated complement cytotoxicity against the L2C cells whereas only that of subclass IgG2 mediated K-cell cytotoxicity; the effector arms were rabbit complement and sheep peripheral leucocytes, respectively.

Animals↗

PubMed2004

The influence of enamel matrix derivative associated with insulin-like growth factor-I on periodontal ligament fibroblasts.

BACKGROUND: Enamel matrix derivative (EMD) has recently been shown to promote periodontal regeneration in vivo. Insulin-like growth factor-I (IGF-I) is a potent modulator of periodontal regeneration stimulating cell proliferation, differentiation, synthesis of type I collagen, and non-collagenous proteins. However, the biochemical effects of these factors on periodontal ligament (PDL) fibroblasts are not completely understood. The objective of the present study was to evaluate the effect of EMD, IGF-I, and the combination of these two factors on the proliferation, adhesion, migration, and expression of type I collagen in PDL fibroblasts. METHODS: The proliferation rate was measured by automated cell counting and immunohistochemical expression of proliferating cell nuclear antigen (PCNA). The cell adhesion was analyzed by a colorimetric assay and cell migration was measured in Boyden chambers. Type I collagen expression and production was determined by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. RESULTS: The results indicated that the proliferation of PDL fibroblasts was significantly stimulated by EMD and EMD plus IGF-I in a dose- and time-dependent manner. EMD, IGF-I, and the combination of both factors had no effects on cellular migration and adhesion or expression and production of type I collagen. CONCLUSION: Our results showed that EMD, IGF-I, and the combination of both factors stimulated PDL fibroblast proliferation, whereas these factors did not affect adhesion, migration, or expression of type I collagen of these cells.

Adolescent↗

PubMed2006

Shear-induced parallel-to-perpendicular orientation transition in the amphiphilic lamellar phase: a nonequilibrium molecular-dynamics simulation study.

The present work is devoted to a study of the shear-induced parallel-to-perpendicular orientation transition in the lamellar system by the large-scale nonequilibrium molecular-dynamics (NEMD) simulation. An effective generic model-A2B2 tetramer for amphiphilies is used. The NEMD simulation produces unambiguous evidence that undulation instability along the vorticity direction sets in well above a critical shear rate and grows in magnitude as the shear rate is further increased. At a certain high shear rate, the coherent undulation instability grows so large that defects are nucleated and the global lamellar monodomain breaks into several aligned lamellar domains. Subsequently layers in these domains rotate into the perpendicular orientation with the rotation of chains towards the y direction, merge into a global perpendicular-aligned lamellar monodomain, and organize into a perfect well-aligned perpendicular lamellar phase by the migration and annihilation of edge dislocations and disclinations. The macroscopic observable viscosity as a function of time or shear rate is correlated with the structural response such as the mesoscopic domain morphology and the microscopic chain conformation. The onset of undulation instability concurs with the start-up of shear-thinning behavior. During the orientation transformation at the high shear rate, the complex time-dependent thixotropic behavior is observed. The smaller viscosity in the perpendicular lamellar phase gives an energetic reason for the shear-induced orientation transition.

Journal Article↗

PubMed2005

A role of STAT3 in Rho GTPase-regulated cell migration and proliferation.

Rho family GTPases and STAT3 act as mediators of cytokine and growth factor signaling in a variety of cellular functions involved in inflammation, tumorigenesis, and development. In the course of searching for their functional connections, we found by using STAT3 knock-out mouse embryonic fibroblasts that RhoA, Rac1, and Cdc42 could cause nonspecific activation of STAT3 promoter-driven luciferase reporter in the absence of STAT3, raising concerns to a body of literature where STAT3 was associated with Rho GTPases based on the reporter system. We also found that although active RhoA, Rac1, and Cdc42 could all mediate Ser-727 and Tyr-705 phosphorylation and nuclear translocation of STAT3, the Rho GTPases were able to induce STAT3 activation independently of the interleukin-6 autocrine pathway, and active RhoA, Rac1, or Cdc42 could not form a stable complex with STAT3 as previously suggested, indicating an unappreciated mechanism of STAT3 activation by the Rho GTPases. The RhoA-induced STAT3 activation partly depended on Rho-associated kinase (ROK) and involved multiple effector signals as revealed by the examination of effector domain mutants of RhoA. Genetic deletion of STAT3 led to a loss of response to RhoA in myosin light chain phosphorylation and actin stress fiber induction but sensitized the cells to RhoA or ROK-stimulated cell migration. STAT3 was required for the RhoA-induced NF-kappaB and cyclin D1 transcription and was involved in NF-kappaB nuclear translocation. Furthermore, loss of STAT3 expression inhibited RhoA-promoted cell proliferation and blocked RhoA or ROK induced anchorage-independent growth. These phenotypic changes in STAT3-/- cells could be rescued by reconstituting STAT3 gene. Our studies carried out in STAT3 null cells demonstrate unambiguously that STAT3 represents an essential effector pathway of Rho GTPases in regulating multiple cellular functions including actin cytoskeleton reorganization, cell migration, gene activation, and proliferation.

Actins↗

PubMedDate not supplied

Hydrostatic pressure effects on eel mitochondrial functioning and membrane fluidity.

Aerobic metabolism which is required for long swimming activities during the eel's spawning migration at depth, is a potential target for pressure effects due to its components located in the inner mitochondrial membrane (respiratory chain and oxidative phosphorylation). Previous studies have evidenced that eels are able to acclimatize to pressure through membrane fluidity adjustment. However these studies were performed on the premigratory stage (yellow stage), which never encounters high pressure. Metamorphosis (silvering) seems to preadapt eels (at the silver stage) to most of the environmental changes they will encounter during migration. Is it also true for pressure resistance? This study shows that yellow eels exhibit a higher pressure sensitivity than silver eels (compression effects). The acclimatization period (21 days at 10.1 MPa) cancels the differences in pressure sensitivity and in aerobic metabolism observed at 0.1 MPa between the two stages. The mechanisms, which take place in yellow eels during acclimatization to high pressure, appear to be already present in silver eels before pressure exposure. Indeed at 0.1 MPa, silver eels exhibit higher membrane fluidity and proportions of membrane polyunsaturated fatty acids. Metamorphosis, by improving membrane fluidity, seems to allow silver eels to cope with hydrostatic pressure without spending energy in acclimatization processes.

Acclimatization↗

PubMed1976

A kindred with hemoglobin Lepore.

Four members from three generations of a family of Italian descent were found to have hemoglobin (Hb) Lepore trait. The four affected members were only slightly anemic, yet had definite hypochromic and microcytic red blood cells (RBC). Electrophoresis of hemoglobin demonstrated an abnormal non-sickling hemoglobin of 11% to 14% concentration that migrated like Hb S at alkaline pH. Amino acid analysis confirmed the identity of the abnormal component as Hb Lepore; the non-alpha chain was a fused delta-beta-chain with a crossover between residues 87 and 116. Hemoglobin Lepore trait should be considered in any patients with clinical and laboratory findings consistent with beta-thalassemia trait and with a 10% to 15% concentration of an abnormal nonsickling hemoglobin that migrates like Hb S.

Adolescent↗

PubMed2004

Factor VII-activating protease (FSAP) inhibits growth factor-mediated cell proliferation and migration of vascular smooth muscle cells.

The factor VII activating protease (FSAP) is a serine-protease present in human plasma that serves to activate single-chain plasminogen activators, as well as coagulation factor VII. FSAP was localized within atherosclerotic lesions, and a genetic polymorphism in FSAP is associated with carotid stenosis. Hence, this study was conducted to gain broader insights into the cellular effects of FSAP on vascular smooth muscle cells (VSMC). DNA synthesis and cell proliferation assays revealed an inhibitory action of FSAP on platelet-derived growth factor BB (PDGF-BB)-mediated proliferation of VSMC. FSAP also inhibited PDGF-BB-induced migration of VSMC. These cellular effects of FSAP could be neutralized by an anti-FSAP mAb as well as by protease inhibitors such as aprotinin or a chloromethylketone inhibitor. Moreover, unfractionated heparin promoted the antiproliferative effect of FSAP on VSMC and was essential for the inhibition of VSMC migration. FSAP inhibited PDGF-BB binding to human VSMC and concomitantly blocked PDGF-BB-dependent phosphorylation of mitogen activated protein kinase p42/p44 and tyrosine phosphorylation of other proteins. These results unravel a new function of FSAP as an inhibitor of the proatherogenic phenotype of vascular smooth muscle.

Arteriosclerosis↗

PubMed2004

Anti-Gal IgG potentiates natural killer cell migration across porcine endothelium via endothelial cell activation and increased natural killer cell motility triggered by CD16 cross-linking.

Xenoreactive antibodies (Ab) are important for the development of acute vascular rejection (AVR) of xenografts characterized by monocytes, natural killer (NK) cells and neutrophils infiltrating the graft. The mechanisms by which anti-galactose alpha 1,3galactose (alpha-Gal) IgG influence NK cell migration across porcine aortic endothelium (PAEC) were investigated. NK cell migration across PAEC increased in the presence of anti-alpha-Gal IgG. Anti-alpha-Gal IgG exposure activated PAEC as shown by an increased expression of CD62E and CD106. NK cells adhered, spread and showed motile forms on plastic surfaces coated with human IgG, IgG Fc and on mAb against CD16, but not on mouse IgG or BSA, suggesting that CD16 cross-linking can mediate increased adhesiveness. Increased NK cell motility was observed on Boyden filters coated with human IgG, IgG Fc, and mAb against CD16 and the alpha 4, alpha 5, alpha L, beta 1 and beta 2 integrin chains. No motile response was seen on mouse IgGor CD7, CD56 and alpha 6 integrin mAb. NK cell migration on human IgG and anti-CD16 Ab was blocked by anti-CD16 or anti-beta 2, but not anti-beta 1 Ab, implying that the motile response triggered by CD16 cross-linking is mediated via beta 2 integrins. Preformed or induced anti-alpha-Gal IgG may therefore contribute to AVR by stimulating innate immune cell infiltration of the graft.

Animals↗

PubMed2001

Invariant chain induces B cell maturation by activating a TAF(II)105-NF-kappaB-dependent transcription program.

Early stages of B cell development occur in the bone marrow, resulting in formation of immature B cells. From there these immature cells migrate to the spleen where they differentiate to mature cells. This final maturation step is crucial for the B cells to become responsive to antigens and to participate in the immune response. Recently, invariant chain (Ii), a major histocompatibility complex class II chaperone, as well as the transcription factors c-Rel and p65/RelA, were found to play a role in the final antigen-independent differentiation stage of B cells in the spleen. In this study, we investigated a possible link between Ii-dependent B cell maturation and the NF-kappaB pathway. Our studies indicate that Ii-induced B cell maturation involves activation of transcription mediated by the NF-kappaB p65/RelA homodimer and requires the B cell-enriched coactivator TBP-associated factor (II)105.

Animals↗

PubMedDate not supplied

Identification of myosin heavy chain in Saccharomyces cerevisiae.

Motility in biological systems is expressed in a variety of ways, such as cytoplasmic streaming, cell shaping, nuclear migration and muscle contraction. These functions are thought to be mediated by structural proteins, for example, myosin, actin and tubulin. The involvement of myosin in muscle contraction is well documented and this protein is implicated in generating the cleavage forces during cytokinesis in some non-muscle cells. Here, we report the isolation of a protein similar to myosin as judged by its biochemical and immunological properties, from the yeast Saccharomyces cerevisiae. Parts of the protein have been conserved through evolution at the protein and DNA sequence levels. The presence of this protein in the region bordering mother cell and bud, as revealed by immunofluorescence, suggests that it is involved in cell division.

Actomyosin↗

PubMedDate not supplied

[Newcastle disease virus in the populations of wild birds in the south of the Primorye Territory in the period of autumn migrations in 2001-2004].

The paper presents the results of molecular virological monitoring of Newcastle disease virus (NDV) by reverse-polymerase chain reaction (followed by sequence of F-gene fragment 374 p.n.) and chick embryo isolation of samples from the avian cloacal swabs collected in the south of the Primorye Territory in September-October 2001-2004. It shows that before 2004, there were only slightly pathogenic variants of NDV of genotype 1 in this region and in 2004 they were added by highly pathogenic variants of subtypes 3a and 5b. The impact of landscaping features of the south of the Primorye Territory on the environment of NDV is discussed.

Animals↗

PubMed1994

Deficiency in the A-subunit of coagulation factor XIII: two novel point mutations demonstrate different effects on transcript levels.

Congenital deficiency in coagulation factor XIII is a rare autosomal recessive bleeding disorder. Although the defect was characterized over 30 years ago, little is known about the molecular basis of the disorder. Here, we show two novel point mutations in the gene of the A-subunit of factor XIII in the genetically isolated population of Finland. All eight factor XIII-deficient families identified in Finland were studied. The exons of the gene of A-subunit were amplified individually by polymerase chain reaction and subsequently screened by single-strand conformation polymorphism. Sequence analysis of the abnormally migrating fragments showed two point mutations resulting in an amino acid alteration. A C-to-T transition at Arg-661 in exon XIV created a premature stop codon. This mutation was detected in six of the eight families, thus being the major alteration causing FXIII deficiency in Finland. In two of the six families, the patients were compound heterozygotes with the Arg-661-Stop mutation in one allele and either a T-to-C point mutation in exon VI or a thus far uncharacterized mutation in the other allele. The T-to-C transition in exon VI resulted in a substitution of threonine for methionine 242. The transition was found in one family only, where it was in the heterozygote form combined with the Arg-661-Stop mutation. To evaluate the consequences of these mutations, steady-state FXIII mRNA levels were quantitated by solid-phase minisequencing. In addition to the termination of translation 70 amino acids before the initial stop codon, the Arg-661-Stop mutation causes a 10- to 30-fold reduction in FXIII mRNA levels. This is also likely to result in a low translation level in the truncated polypeptide. In contrast, Met-242-Thr mutation does not seem to affect the level of mRNA. Here, the absence of a functional and immunodetectable protein is probably caused by an altered conformation of the mutant polypeptide, resulting in early degradation of the defective protein.

Adolescent↗

PubMed2003

Expression and function of the vascular endothelial growth factor receptor FLT-1 in human eosinophils.

Vascular endothelial growth factor (VEGF) is highly expressed in the airway of patients with asthma. Whether VEGF affects eosinophil function in vitro and if VEGF receptors are involved was tested. Eosinophils were from venous blood of healthy donors. Cell migration was studied by micropore filter assays. Signaling mechanisms required for VEGF-dependent migration were tested using signaling enzyme blockers. Expression of flt-1 and KDR/flk-1 mRNA in eosinophils was demonstrated in reverse transcriptase-polymerase chain reaction, and receptor expression was investigated by fluorescence-activated cell sorting analysis. Eosinophil cationic protein release was measured in eosinophil supernatants by enzyme-linked immunosorbent assay. VEGF significantly stimulated eosinophil chemotaxis via activation of protein kinase C and phosphatidylinositol 3'-kinase. The effect on migration was reversed by an antibody against VEGF receptor flt-1, but not by an antibody against KDR/flk-1. Expression of VEGF receptor flt-1 mRNA was shown and synthesis of VEGF receptor in eosinophils is suggested by detection of VEGF receptor immunoreactivity on the cell surface. Data suggest that VEGF receptor flt-1 is expressed by eosinophils whose activation with VEGF stimulates directed migration and release of eosinophil cationic protein. Thus, VEGF may play an important role in the modulation of eosinophilic inflammation.

Antibodies↗

PubMed2002

Invariant chain induces B cell maturation in a process that is independent of its chaperonic activity.

Early stages of B cell development take place in the bone marrow, resulting in formation of immature B cells, which migrate to the spleen for their final differentiation into mature cells. This final maturation step is essential for B cells to become responsive to antigens and to participate in the immune response. Previously, we showed that the MHC class II chaperone, invariant chain (Ii), controls the differentiation of B cells from the immature to the mature stage. In this study, by generating transgenic mice expressing truncated Ii lacking its luminal domain, we could dissect the chaperonin activity of Ii from its role in B cell maturation. We demonstrate in vivo that Ii N-terminal domain is directly involved in the maturation of B cells and is sufficient to promote B cell differentiation.

Animals↗

PubMed1998

Kar9p is a novel cortical protein required for cytoplasmic microtubule orientation in yeast.

kar9 was originally identified as a bilateral karyogamy mutant, in which the two zygotic nuclei remained widely separated and the cytoplasmic microtubules were misoriented (Kurihara, L.J., C.T. Beh, M. Latterich, R. Schekman, and M.D. Rose. 1994. J. Cell Biol. 126:911-923.). We now report a general defect in nuclear migration and microtubule orientation in kar9 mutants. KAR9 encodes a novel 74-kD protein that is not essential for life. The kar9 mitotic defect was similar to mutations in dhc1/dyn1 (dynein heavy chain gene), jnm1, and act5. kar9Delta dhc1Delta, kar9Delta jnm1Delta, and kar9Delta act5Delta double mutants were synthetically lethal, suggesting that these genes function in partially redundant pathways to carry out nuclear migration. A functional GFP-Kar9p fusion protein localized to a single dot at the tip of the shmoo projection. In mitotic cells, GFP-Kar9p localized to a cortical dot with both mother-daughter asymmetry and cell cycle dependence. In small-budded cells through anaphase, GFP-Kar9p was found at the tip of the growing bud. In telophase and G1 unbudded cells, no localization was observed. By indirect immunofluorescence, cytoplasmic microtubules intersected the GFP-Kar9p dot. Nocodazole experiments demonstrated that Kar9p's cortical localization was microtubule independent. We propose that Kar9p is a component of a cortical adaptor complex that orients cytoplasmic microtubules.

Amino Acid Sequence↗

PubMed1998

CD4+ T cells from 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rodents migrate to the recipient's colon upon transfer; down-regulation by CD8+ T cells.

CD4+ T cells play an important role in the aetiology of inflammatory bowel disease (IBD), but it is not clear which factor(s) cause activation of these cells. The aim of this study was to examine the effects of adoptive transfer of splenic (CD4+) T cells from TNBS/ethanol-sensitized donor rats to naive recipients and the migration pattern of transferred T cells. For the transfer experiments, colitis was induced in rats by colonic administration of TNBS/ethanol. Seventeen days later, either total splenic T cells or CD4+, or CD8+ T cells were transferred to naive recipients. At days 1, 2 and 3 after transfer, the recipients were killed and the migration pattern of the transferred T cells was studied, as well as inflammatory cells in several organs, including the colon. To determine cytokine profiles of the T cells, colitis was induced in mice. Therefore, different combinations of 2,4-dinitrobenzene sulfonic acid (DNBS) in ethanol or saline, or ethanol alone were intrarectally administered. At day 9 after induction of colitis, mice were killed and cytokine profiles in the colon were studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. The results show that CD4+ T cells from donor rats with TNBS/ethanol-induced colitis migrate in particular to the colon upon transfer to naive recipients, and that this process is down-regulated by CD8+ T cells. This migration is probably caused by T cell recognition of the colonic bacterial flora and initiates an inflammatory reaction in the recipient's colon, characterized by an increase of the recipient's own T cells, macrophages, and neutrophils. In the mice experiments we showed that a second administration of DNBS/ethanol or ethanol alone, which presumably causes bacterial translocation, results in increased numbers of T cells into the colon, accompanied by an increase in Th1 cytokines. These data suggest that Th1 cells recognize the colonic bacterial flora.

Adoptive Transfer↗