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PubMed1987

[Immune barriers of the mucous membrane of the upper respiratory and digestive tracts].

The mucosa that lines the upper respiratory and digestive pathways is protected by a secretory immune system which is under complex and only partly understood immunoregulatory control. B cells of relatively immature memory clones with a potential for J-chain expression, are initially stimulated in mucosa-associated lymphoid tissue (probably including the tonsils) and migrate thereafter through lymph and blood to glandular sites where they are subjected to terminal differentiation and become immunoglobulin (Ig)-producing immunocytes. Most locally produced Ig is normally dimeric IgA which is selectively transported through the serous type of glandular cells by means of an epithelial receptor protein called the secretory component (SC). IgM is also subjected to SC-mediated transport. In patients with selective IgA deficiency, secretory IgA is lacking but it may be satisfactorily replaced by protective secretory IgM. In other IgA-deficient patients, however, immunoregulatory compensation gives rise to a large number of IgD-producing cells in respiratory mucosa. IgD cannot act as a secretory antibody and these patients are prone to have recurrent infections. These observations show that there are large individual variations in the secretory immune system.

Antibody Formation↗

PubMed1993

Mechanism of action of antimalarial drugs: inhibition of antigen processing and presentation.

Recent studies have elucidated the steps involved in the association of antigenic peptides with major histocompatibility complex (MHC) encoded proteins and have suggested how antimalarial compounds might influence this important site of immune activation. These steps of antigen presentation in the macrophage (or other antigen-presenting cells) include: (a) the partial proteolytic degradation of endogenous and exogenous proteins into peptides within the lysosome; (b) the synthesis of MHC class II (i.e. HLA-D associated) alpha, beta, and invariant (Ii) chains in the endoplasmic reticulum; (c) the initial association of alpha-Ii and beta-Ii chains in the endoplasmic reticulum and the transport of these complexes to the primary endosome; (d) the fusion of lysosomal vacuoles and endosomal vacuoles, allowing the mixtures of lysosomal enzymes, peptides, alpha-Ii and beta-Ii; (e) the displacement of Ii chains by peptides to form alpha-beta-peptide complexes in the endosome; and (f) the migration of alpha-beta-peptide complexes to the macrophage cell surface where they can stimulate CD4 T cells, resulting in release of cytokines. A low pH is required for digestion of the protein by acidic hydrolases in the lysosome, for assembly of the alpha-beta-peptide complex and for its transport to the cell surface. Chloroquine and hydroxychloroquine are weak diprotic bases that can diffuse across the cell membrane and raise the pH within cell vesicles. This background provides the underlying basis for the theory that antimalarials may act to prevent autoimmunity by the following putative mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

[Effects of CD151 on migration of human tongue squamous carcinoma cell line Tca8113].

BACKGROUND & OBJECTIVE: Over-expression of CD151 gene in tumor tissues may be associated with metastasis and poor prognosis of cancer, but the mechanism is unknown. This study was designed to determine the effects of CD151 gene on migration of human tongue squamous carcinoma cell line Tca8113. METHODS: Functional fragment of CD151 gene was amplified by reverse transcription-polymerase chain reaction (RT-PCR), and inserted into plasmid adeno-associated virus (pAAV) vector in sense direction and antisense direction to construct rAAV-CD151 and rAAV-antiCD151, the virus titers were determined by dot blot. Two weeks after transfection, protein level of CD151 in Tca8113 cells was detected by Western blot, the effect of CD151 on migration of Tca8113 cells was detected by Transwell chambers. RESULTS: Titer of rAAV-CD151 was 2x10(11) pfu/ml, titer of rAAV-antiCD151 was 1x10(11) pfu/ml. Transfection of rAAV-CD151 increased expression of CD151 in Tca8113 cells by 108% of control cells, while transfection of rAAV-antiCD151 decreased expression of CD151 in Tca8113 cells by 79% of control cells. Migrated cells count was significantly higher in rAAV-CD151-transfected cells (93.6+/-11.6), and lower in rAAV-antiCD151-transfected cells (24.0+/-4.4) than in untransfected and rAAV-GFP-transfected cells (53.0+/-6.6 and 46.0+/-7.0, P<0.05). CONCLUSIONS: It is an important molecular mechanism of tumor metastasis that over-expression of CD151 promotes migration of tumor cells. rAAV-antiCD151, a novel therapeutic tool, can specifically reduce the expression of CD151, and inhibit migration of tumor cells.

Antigens, CD↗

PubMed2005

Opposing roles for p21(waf1/cip1) and p27(kip1) in enterocyte differentiation, proliferation, and migration.

BACKGROUND: Originating from proliferating stem cells of the intestinal crypt, enterocytes differentiate as they migrate up the crypt-villus axis. A regulatory role of the cyclin-dependent kinase inhibitors p21(waf1/cip1) and p27(kip1) in these processes has been suggested by in vitro models. We sought to determine the effect of p21(waf1/cip1) and p27(kip1) deficiency on enterocyte differentiation, proliferation and migration. METHODS: Three strains of mice including control (C57Bl/6), p27(kip1)-null, and p21(waf1/cip1)-null were studied. Enterocyte differentiation was evaluated by immunostaining for intestinal alkaline phosphatase, by colorimetric assaying for intestinal alkaline phosphatase and sucrase enzyme activity, and by polymerase chain reaction for intestinal fatty acid-binding protein and villin-messenger RNA in enterocytes extracted by laser capture microdissection. Rates of enterocyte proliferation and migration were determined by 5-bromo 2-deoxyuridine immunostaining after a 50% small-bowel resection (SBR). RESULTS: Compared with controls, p27(kip1)-null mice demonstrated minimal differentiation but maintained a normal proliferative response to SBR. Contrarily, p21(waf1/cip1)-null mice demonstrated greater enterocyte differentiation without significant increases in enterocyte proliferation after SBR. CONCLUSIONS: These findings suggest that p21(waf1/cip1) and p27(kip1) have distinctive and opposing roles in the pathogenesis of enterocyte differentiation, proliferation, and migration.

Animals↗

PubMedDate not supplied

Reptation-breathing theory of pulsed electrophoresis: dynamic regimes, antiresonance and symmetry breakdown effects.

We apply the concepts of tube and reptation to the pulsed electrophoresis of DNA, considering both biased reptation and "breathing" modes (internal modes of the chain). Using suitable preaveraging approximations, analytical expressions are derived which relate displacement in crossed field electrophoresis to molecular weight, field strength, field period, pore size of the gel, and the angle between the field. These expressions provide scaling laws for the change of mobility when one (or more) of the parameters is varied as well as "universal" velocity versus molecular weight versus pulse time curves. These results are quantitatively compared with experiments. At some point which depends on field angle, field strength and chain length, however, we predict a failure of this model due to symmetry breakdown and loss of ergodicity. Qualitatively, this should lead to considerable band spreading and/or splitting of the highest DNA bands into two bands migrating sideways from the diagonal. The case of field inversion is also investigated. It is shown that only breathing modes can explain the strong differences in mobility experienced by chains of different length when opposite fields of equal amplitude are applied: the "trapping" of chains in conformations of low mobility is associated with an antiresonance-like coupling between the external field and the internal modes.

Chromosomes↗

PubMed1995

Neolactoglycosphingolipids, potential mediators of corneal epithelial cell migration.

Cell migration is a fundamental process of wound repair in biological systems. In an attempt to identify plasma membrane glycoconjugates which mediate cell migration, migrating and nonmigrating rabbit corneal epithelia were analyzed for reactivity with monoclonal antibodies (mAbs) specific for unsubstituted N-acetyl-lactosamine (mAb 1B2), Le(x) (mAbs 7A and MMA), and sialyl Le(x) (mAb CSLEX1) carbohydrate chains of neolactoglycoconjugates. Immunohistochemical analysis indicated that regardless of whether the epithelia analyzed were from corneas of animals in vivo, corneas in organ culture, or cells in tissue culture, migrating cells stained intensely with mAb 1B2, whereas nonmigrating cells either did not stain or stained only weakly. mAbs MMA and 7A stained migrating epithelium as well as basal and middle cell layers of normal, nonmigrating epithelium. mAb CSLEX1 did not stain wounded corneas but stained the superficial cell layer of normal corneal epithelium. Biochemical analyses by TLC immunostaining revealed the presence of three mAb 1B2-reactive glycosphingolipids (GSL), neolactotetraosyl-(nLc4, paragloboside), neolactohexaosyl- (nLc6), and neolacto-octaosylceramide (nLc8) in migrating epithelia. In contrast, nonmigrating epithelia contained only trace amounts of these glycolipids. Exogenous addition of nLc4, but not various other GSLs including a Le(x)-GSL (SSEA-1), stimulated re-epithelialization of wounds in an experimental model of corneal epithelial wound healing. Moreover, re-epithelialization of wounds was significantly inhibited by mAb 1B2 but not by mAb MMA. The data suggest that neolacto-GSLs of corneal epithelium may be among the molecules which mediate healing of corneal epithelial wounds by influencing cell migration.

Animals↗

PubMed1987

Heparan sulfate proteoglycans of human lung fibroblasts. Structural heterogeneity of the core proteins of the hydrophobic cell-associated forms.

Heparan sulfate proteoglycans (HSPG) were solubilized from human lung fibroblast monolayers with detergent. Presumptive membrane-associated forms displaying hydrophobic properties were purified by gel filtration on Sepharose CL-4B, by ion-exchange chromatography on Mono Q and by incorporation in lipid vesicles. The HSPG preparations were 125I-iodinated and treated with heparitinase before sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Five radiolabeled proteins with apparent molecular weights of 125,000, 90,000, 64,000, 48,000, and 35,000 were visualized by autoradiography. A sixth protein, identified in nonreduced 125I-HSPG preparations, appeared as a non-HS chain-bearing Mr 35,000 peptide which was disulfide-linked to an HS chain-bearing peptide of similar size. This multiplicity of core proteins did not seem to result from proteolysis during the heparitinase treatment itself, since some of the core proteins migrated independently during gel filtration before heparitinase digestion. Moreover, heparitinase digestion of 125I-HSPG purified by affinity chromatography on an immobilized monoclonal antibody yielded only the Mr 64,000 protein. Alternative depolymerizations of the HS chains by heparinase or HNO2 also yielded multiple protein bands. These results imply that heterogeneity of the core protein moiety may be a genuine property of the hydrophobic HSPG of human lung fibroblasts. The occurrence of multiple integral membrane HSPG forms may be relevant for the multiple functions that have been ascribed to cell-surface HSPG.

Cells, Cultured↗

PubMed1995

The laminin alpha 1 chain Ile-Lys-Val-Ala-Val (IKVAV)-containing peptide promotes liver colonization by human colon cancer cells.

Laminin, a major basement membrane-specific glycoprotein, promotes the attachment, migration, and invasion of a variety of tumor cells. Since laminin is present in the perisinusoidal matrix of the liver, we studied its effects on liver colonization by human colon cancer cells (HM7, LiM6) previously shown to have liver-metastasizing ability in athymic mice. These malignant cells expressed high levels of a 32-kDa laminin-binding protein on Western blot analysis when compared to the low metastatic parental cell line. Coinjection of laminin alpha chain-derived peptides which contain the amino acid sequence Ile-Lys-Val-Ala-Val (IKVAV) significantly stimulated liver colonization as determined by liver weight (P < 0.005) and number of tumor nodules (P < 0.02) 3 weeks after splenic-portal inoculation into nude mice. No stimulation was seen with a control peptide containing the same amino acids but in a scrambled sequence. In contrast, the Tyr-Ile-Gly-Ser-Arg peptide from the laminin beta 1 chain significantly inhibited HM7 liver colonization. These differences were not due to alterations in the number of cells initially reaching the liver as determined by injection of [125I]iododeoxyuridine-labeled tumor cells, but retention in the liver was stimulated by the IKVAV-containing peptides. Flow analysis indicated that the IKVAV peptide may act, in part, by stimulating homotypic adhesion of tumor cells. These data suggest that interactions of colon cancer cells with the IKVAV site on laminin may play a role in the formation of metastatic foci in the liver through cell-cell or cell-substratum interactions which promote metastasis.

Adenocarcinoma↗

PubMed1997

Increased diameters of collagen fibrils precipitated in vitro in the presence of decorin from various connective tissues.

Proteoglycans were isolated from bovine skin, sclera, deep flexor tendon and the periphery of the temporomandibular joint disc with urea. Decorin was purified from each of these extracts by ion-exchange, hydrophobic-interaction and gel-filtration chromatography. Purities were assessed by amino acid analysis and by sodium dodecylsulphate polyacrylamide gel electrophoresis (SDS-PAGE) of the protein cores released by digestion with chondroitin-ABC-lyase. In these respects the decorins were indistinguishable. However the glycosaminoglycan chains released by digesting the proteoglycans with papain varied widely in mobility on SDS-PAGE: that from skin decorin migrating fastest and that from tendon decorin slowest. The effects of each of the decorins on collagen fibrillogenesis in vitro were similar, all reducing the rate of fibril growth (by 55 to 71%, depending on the source of the proteoglycan) and increasing the diameters of the fibrils formed (by 27 to 66%). Core protein alone, isolated from skin decorin, reduced the rate of fibril growth as effectively as intact decorin, but had no effect on the diameter of fibrils formed. The dermatan sulphate chain and the protein thus appear to play different roles in the interaction of intact decorin with collagen. These data suggest that decorin found in fibrous connective tissues may increase Type I collagen fibril diameters, resulting in tissues that are better able to withstand tensile forces.

Animals↗

PubMed2004

Mobilization of opioid-containing polymorphonuclear cells by hematopoietic growth factors and influence on inflammatory pain.

BACKGROUND: Leukocytes can control inflammatory pain by secretion of opioid peptides, stimulated by cold-water swimming or local injection of corticotropin-releasing factor, and subsequent activation of opioid receptors on peripheral sensory neurons. This study investigated whether mobilization of polymorphonuclear cells (PMN) by granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) enhances immigration of opioid-containing PMN and peripheral opioid analgesia in rats with Freund complete adjuvant-induced hind paw inflammation. METHODS: In circulating PMN of rats treated with G-CSF+SCF and sham-treated rats, opioid peptide content was measured by radioimmunoassay. Expression of adhesion molecules (CD62L, CD49d, CD18), in vitro migration in the Boyden chamber, and infiltrating leukocytes were analyzed by flow cytometry. Chemokine messenger RNA transcription was quantified by LightCycler polymerase chain reaction. Paw pressure threshold was measured at baseline, after cold-water swimming, and after injection of corticotropin-releasing factor. RESULTS: G-CSF+SCF treatment increased circulating PMN (11-fold, P < 0.05). Mobilized PMN had decreased content of beta-endorphin but not of Met-enkephalin per cell, down-regulation of CD62L, up-regulation of CD49d (but no change in CD18), and reduced migration toward higher chemokine concentrations (all P < 0.05). In the paw, one of four chemokine messenger RNAs was significantly expressed during the first 2 h of inflammation (P < 0.05), immigration of PMN and opioid-containing cells was slightly increased (1.5-fold, P < 0.05), and baseline paw pressure threshold, as well as paw pressure threshold increases induced by corticotropin-releasing factor and cold-water swimming, were unchanged (P > 0.05). CONCLUSIONS: G-CSF+SCF mobilized circulating opioid-containing PMN but had a minor influence on cell migration and peripheral analgesia, probably because of the low expression of chemokines in the inflamed paw and one of the decreased beta-endorphin content in PMN.

Animals↗

PubMed1991

Identification of the glucocorticoid suppressible mitogen from rat hepatoma cells as an angiogenic platelet-derived growth factor A-chain homodimer.

We have previously shown that BDS.1 rat hepatoma cells are hypersensitive to the antiproliferative effects of glucocorticoids, and secrete a glucocorticoid suppressible mitogenic activity (denoted GSM). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that GSM purified to near homogeneity migrated as a 28-kDa protein under nonreducing conditions and as a single 15-kDa polypeptide in the presence of sulfhydryl reducing agents suggesting a homodimeric structure. Anti-platelet-derived growth factor (PDGF) A-chain specific antibodies selectively immunodepleted the mitogenic activity which can be extracted from nonreducing gels in the 26-30-kDa fraction and, in Western blots, recognized the 15-kDa reduced form of GSM. Western blot analysis further showed that dexamethasone suppressed the level of secreted PDGF A-chain protein in BDS.1 cells but not in glucocorticoid receptor-deficient hepatoma cells. Northern blots revealed that dexamethasone reduced expression of the PDGF A-chain 2.3- and 1.7-kilobase transcripts in proportion to the level of detectable PDGF-AA protein. Similarly to PDGF-AA, the hepatoma cell-derived GSM has a potent angiogenic activity. Taken together, our results demonstrate that the predominant glucocorticoid suppressible mitogen secreted from rat hepatoma cells is a PDGF A-chain homodimer and suggest that in vivo glucocorticoids may potentially regulate hepatoma growth by modulating PDGF-stimulated tumor vascularization.

Animals↗

PubMed2004

CXCR4 and CXCL12 (SDF-1) in prostate cancer: inhibitory effects of human single chain Fv antibodies.

PURPOSE: Metastasis is a major cause of morbidity in prostate cancer (PCa). Several studies have shown that the chemokine receptor CXCR4 and its ligand, CXCL12 (stromal cell-derived factor-1), regulate tumor cell metastasis to specific organs. Recently, it was demonstrated that CXCL12 enhances PCa cell adhesion, migration, and invasion, implicating CXCR4 in PCa metastasis. In this study, we examined the inhibitory effects of anti-CXCR4 antibodies on CXCL12-mediated PCa cell activities. EXPERIMENTAL DESIGN: We developed fully human single chain Fv antibodies (scFv), Ab124 and Ab125, against CXCR4 using the yeast two-hybrid system. We performed immunofluorescent staining, flow cytometry, and ELISA-binding assays to measure scFv binding to PCa cells. We also examined the effects of scFv on CXCL12-mediated calcium mobilization, cell migration, and invasion. RESULTS: Our results confirmed that PCa cell lines express cell-surface CXCR4. Real-time quantitative reverse transcription-PCR and immunohistochemical staining also verified that CXCR4 is expressed in primary cultures of prostate epithelial cells from adenocarcinomas and in human prostate tissues. Ab124 and Ab125 demonstrated specific binding to PCa cell lines by flow cytometry and in binding assays. Preincubation with scFv resulted in significant reduction of CXCL12-induced calcium mobilization in PC-3 and LNCaP cells. Ab124 and Ab125 also inhibited PCa cell migration toward CXCL12, as well as invasion through extracellular matrix gels. CONCLUSIONS: Ab124 and Ab125 inhibit CXCL12-mediated cellular activities by binding the receptor CXCR4. Recombinant scFv are an efficient mode of targeting tumor antigens. Considering the high incidence of PCa, the development of fully human scFv may be a useful therapeutic approach in the prevention and treatment of PCa metastasis.

Breast Neoplasms↗

PubMed1997

Random migration of polymorphonuclear leukocytes induced by GM-CSF involving a signal transduction pathway different from that of fMLP.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) induced random migration of human polymorphonuclear leukocytes (PMNs) but not chemotaxis. Chemoattractants such as N-formyl-methionyl-leucyl-phenylalanine (fMLP), leukotriene B4 (LTB4), and interleukin-8 (IL-8) induced both random migration and chemotaxis. Other inflammatory cytokines, including granulocyte colony-stimulating factor (G-CSF), interleukin 1alpha (IL-1alpha), and tumor necrosis factor alpha (TNF-alpha), did not induce either movement. One-minute exposure of PMNs to GM-CSF was sufficient for the induction of random migration, whereas fMLP-induced random migration required continued presence of fMLP. Inhibitors of phosphatidylinositol 3-kinase (PI3-K), protein kinase C (PKC), and protein tyrosine kinase (PTK) had no effect on random migration induced by GM-CSF, whereas fMLP-induced movements were partially inhibited by PTK inhibitors but not by inhibitors of PI3-K inhibitors nor PKC inhibitors. Myosin light chain kinase inhibitors inhibited movements of PMNs induced by both GM-CSF and fMLP. These findings also imply that some aspects of the signal transduction pathway of GM-CSF leading to random migration is different from that of fMLP. Our findings suggest that cell movements are controlled through diverse signal transduction systems.

Androstadienes↗

PubMed1994

Retrovirus-induced immunosuppression via blocking of dendritic cell migration and down-regulation of adhesion molecules.

Dendritic cells (DC) within tissues may acquire and process antigens, carry them into lymph nodes and cluster and activate T cells. The ability of DC to acquire antigen and to migrate to lymph nodes was estimated during murine retroviral infection caused by Rauscher leukaemia virus (RLV). A novel mechanism of inducing immunodeficiency has now been identified. In mice infected with RLV, DC failed to migrate into lymph nodes following exposure of the skin to the contact sensitizer, fluorescein isothiocyanate. RLV infection of a proportion of DC both in skin and lymph nodes, shown by semi-quantitative polymerase chain reaction (PCR) and down-regulation of expression of adhesion molecules (CD54 and CD44) on the surface of Langerhans' cells, may contribute to the described phenomenon. A failure of DC migration could be an important immunosuppressive mechanism of RLV infection in mice and we speculate on a similar role for DC in human immunodeficiency virus-1 (HIV-1) infection in humans.

Animals↗

PubMed2003

Expression and function of the endothelial protein C receptor in human neutrophils.

Activation of protein C by thrombin bound to thrombomodulin is enhanced by endothelial protein C receptor. This pathway may inhibit inflammation. We investigated effects of protein C and activated protein C on neutrophils as well as whether an endothelial protein C receptor is involved in mediating protein C effects. Neutrophils were from venous blood of healthy donors. Cell migration, respiratory burst, phagocytic activity, and apoptosis were studied by micropore filter assays and fluorometry. Receptor expression was investigated by reverse transcriptase-polymerase chain reaction (PCR) for mRNA, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and autoradiography of immunoprecipitated receptor protein, and fluorescence-activated cell-sorter scanner (FACS) analysis using the anti-endothelial protein C receptor antibody RCR-252. Neither protein C nor activated protein C induced migration, yet both of them inhibited neutrophil chemotaxis triggered by interleukin-8, formyl-Met-Leu-Phe, antithrombin, or C5a. A protein C activation-blocking antibody against endothelial protein C receptor diminished inhibitory effects of protein C or activated protein C on migration. No effect of either protein C preparation was seen in neutrophil's respiratory burst, bacterial phagocytosis, or apoptosis assays. Endothelial protein C receptor immunoreactivity was confirmed on neutrophils by FACS. De novo synthesis is suggested by endothelial protein C receptor mRNA expression as demonstrated by reverse transcriptase PCR and immunoprecipitation SDS-PAGE analyses. Data suggest that an endothelial protein C receptor is expressed by human neutrophils whose active site ligation with either protein C or activated protein C arrests directed cell migration. Inhibitory effects of these components of the protein C pathway on neutrophil function may play a role in the protein C-based treatment of severe sepsis.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2006

Protease-dependent activation of nasal polyp epithelial cells by airborne fungi leads to migration of eosinophils and neutrophils.

CONCLUSIONS: Proteases in fungi interact with nasal epithelial cells and enhance the production of inflammatory cytokines in vitro. These cytokines induced the migration of eosinophils and neutrophils. Protease-activated receptors (PARs) might also play a role in the process of epithelial cell activation. OBJECTIVE: The nasal epithelium is the first barrier encountered by airborne allergens and an active participant in airway inflammation. Fungi have been increasingly recognized as important pathogens in sinusitis and consist of several allergenic proteins. MATERIALS AND METHODS: Nasal polyp epithelial cells were obtained from patients and stimulated with Alternaria, Aspergillus, and Cladosporium. Interleukin-8 (IL-8), granulocyte-macrophage colony stimulating factor (GM-CSF), and regulated on activation normal T expressed and secreted (RANTES) were measured to determine the activation of epithelial cells. Reverse transcriptase-polymerase chain reaction test (RT-PCR) for PAR mRNA expression in nasal epithelial cells was performed. Eosinophil and neutrophil migration was induced with nasal polyp epithelial cells conditioned media (HPECM). RESULTS: Fungi enhanced the production of chemical mediators from nasal epithelial cells. When nasal epithelial cells were activated with fungi, PAR2 and PAR3 mRNAs were more strongly expressed than in nonactivated cells. Eosinophil migration was induced by RANTES and eotaxin, and neutrophil migration was induced by IL-8 in HPECM.

Allergens↗

PubMed1997

Human orosomucoid polymorphism: molecular basis of the three common ORM1 alleles, ORM1F1, ORM1F2, and ORM1*S.

The human orosomucoid (ORM) is controlled by two closely linked loci, ORM1 and ORM2, and two tandem genes, AGP1 and AGP2, encoding the proteins produced by the two loci, have been cloned. In this study the molecular basis of ORM1 polymorphism was investigated. For the detection of mutations the products of the six exons of each gene, amplified by the polymerase chain reaction (PCR), were screened by single-strand conformation polymorphism analysis. Subsequently, the exons with an altered migration pattern were gene-specifically amplified by nested PCR. Sequencing of the gene-specific PCR products showed that the three common ORM1 alleles result from A-->G transitions at the codons for amino acid positions 20 in exon 1 and 156 in exon 5 of the AGP1 gene: ORM1*F1 was characterized by CAG (Gln) and GTG (Val), ORM1*F2, by CAG (Gln) and ATG (Met), and ORM1*S, by CGG (Arg) and GTG (Val). The phylogenesis of the genes encoding these three ORM1 alleles is discussed.

Alleles↗

PubMed2003

Early expression of chicken gonadotropin-releasing hormone-1 in the developing chick.

Gonadotropin-releasing hormone (GnRH), which is essential for reproductive function, is made by neurones that migrate from the nasal region into the brain during early embryonic development. This migration begins in chick when the olfactory pit is formed. This is approximately the time that GnRH neurones can be detected immunocytochemically. The present study investigated (i). how early in development the GnRH gene is expressed and (ii). the sites of its expression. Accordingly, reverse transcriptase-polymerase chain reaction (PCR) and in situ hybridization were performed on chick embryos before gastrulation up until the stage by which GnRH neurones have begun to migrate into the central nervous system. Primers were made to the 5'- and 3'-UTR region of the message for cGnRH-I, the form of the peptide that is essential for reproductive function in the chicken. PCR product was found in all stages and the sequences of products from all stages were identical. Thus, the GnRH gene is expressed continuously throughout embryonic development. In situ hybridization with a digoxygenin labelled riboprobe revealed staining along the primitive streak immediately before gastrulation. In later stages, cGnRH-I gene expression was seen in association with the anterior neural ridge. The expression was subsequently restricted to a narrow, clearly defined region, which is associated with the presumptive nasal cavity and olfactory placode. Later, GnRH neurones could be seen in their migratory routes by both in situ hybridization and immunocytochemistry. Expression of the GnRH gene has been described in preimplantation stages in mammals and there is evidence that the neuropeptide plays a role in formation and maintenance of the placenta. What role (if any) it may play in early avian development remains unknown. The demonstration of sites of GnRH expression during the early period of neurulation suggests that GnRH neurones arise before olfactory placode formation.

Animals↗