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Results for “Cell Lineage”

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At least 271 records · Page 15Linked to original sources

PubMed1986

Epstein-Barr virus immortalization of normal cells of B cell lineage with nonproductive, rearranged immunoglobulin genes.

Most continuous cell lines derived by EBV immortalization of peripheral blood cells are composed of phenotypically mature B lymphocytes, and secrete Ig. Occasionally, EBV-immortalized cell lines have failed to secrete Ig. Expansion and characterization of one of these EBV-induced cell lines, VDS-O, showed that in addition to a lack of Ig secretion, surface and intracytoplasmic Ig were absent. Cell surface phenotyping revealed that VDS-O belongs to the B cell lineage, because it expresses the B cell restricted antigens B1 and B4, while it lacks T cell and monocyte-associated determinants. Analysis of the Ig gene organization in VDS-O revealed that the Ig genes are rearranged for both heavy (gamma) and light (kappa) chains. However, the expected gamma-heavy chain and/or kappa-light chain RNA species were not detected. These findings demonstrate the existence in normal peripheral blood of cells of B cell lineage susceptible to EBV immortalization that have Ig genes that are rearranged but are nonproductive.

Antibody Formation↗

PubMed2003

Establishment and characterization of a spontaneously immortalized mouse ameloblast-lineage cell line.

Tooth development was cooperatively regulated by the epithelial ameloblasts and mesenchymal odontoblasts. Ameloblasts secrete enamel matrix, critical for enamel formation. While there are several reports about establishment of immortalized ameloblast-like cells by introducing viral oncogene, we tried to establish a spontaneously immortalized ameloblast-lineage cell line, maintaining the cell type specific character, including the ability to induce in vitro bio-mineralization. The established cell line (ameloblast-lineage cell; ALC) maintained the expression of several ameloblast specific genes (Amelogenin, Tuftelin, and Enamelin) in long-term culture. They formed calcified nodules after the induction by medium switching from SMEM to DMEM, having high-level alkaline-phosphatase activity. The size and number of calcified nodule formation were enhanced by TGF-beta treatment. Six weeks after sub-cutaneous implantation of ALC to athymic nude mice, we ectopically observed enamel epithelium like structure formation, chondrogenesis, and calcification. These data indicate that ALC is a useful experimental tool to analyze ameloblast character.

Alkaline Phosphatase↗

PubMed2005

Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8(+)CD34(+) T cells from patients with T-cell-lineage acute lymphocytic leukemia.

We investigated CD4(+)CD34(+), CD8(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells from cord blood and from typical patients with T-cell-lineage acute lymphocytic leukemia and T-cell-lineage chronic lymphocytic leukemia in terms of expression and functions of CXCR5/CXCL13. We found that CXCR5 was selectively frequently expressed on T-cell-lineage acute (chronic) lymphocytic leukemia (T-ALL) CD8(+)CD34(+) T cells, but not on T-ALL CD4(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells. CXCR5 was rarely expressed on all types of CD34(+) and CD34(-) CB or T-CLL T cells. CXCL13/B cells attracting chemokine 1 induced significant resistance to TNF-alpha-mediated apoptosis in T-ALL CD8(+)CD34(+) T cells, instead of induction of chemotactic and adhesive responsiveness. A proliferation-inducing ligand expression in T-ALL CD8(+)CD34(+) T cells was upregulated by CXCL13/BCA-1 (B-cell attracting chemokine 1). The CXCR5/CXCL13 pair by means of activation of APRIL (A proliferation-inducing ligand) induced resistance to apoptosis in T-ALL CD8(+)CD34(+) T cells in livin-dependent manner. In this process, cell-cell contact in culture was necessary. Based on our findings, we suggested that there were differential functions of CXCR5/CXCL13 in distinct types of cells. Normal lymphocytes, especially naive B and T cells, utilized CXCR5/CXCL13 for migration, homing, maturation, and cell homeostasis, as well as secondary lymphoid tissue organogenesis. Meanwhile, certain malignant cells took advantages of CXCR5/CXCL13 for infiltration, resistance to apoptosis, and inappropriate proliferation.

Adaptor Proteins, Signal Transducing↗

PubMed1994

Emergence of myogenic and endothelial cell lineages in avian embryos.

The roles of cell cycles and of cell-cell interactions in the emergence of myogenic and endothelial cell lineages were studied in avian embryos using the quail-chicken marker system. Quail embryos were treated with drugs preventing either DNA replication or the movement of cells. Portions of drug-treated or untreated quail blastoderms were grafted into chicken wing buds. After an incubation for an additional 4 to 10 days, the embryos were analyzed for the presence of quail muscle or quail endothelial cells by the Feulgen reaction and by immunostaining. Both cell lineages differ in the time of their commitment as well as in the conditions necessary for their emergence. Muscle cells did not differentiate from unincubated blastoderms nor did they develop from drug-treated blastoderms. These results corroborate that the commitment of myogenic cells occurs during gastrulation and indicate that this commitment requires both DNA replication and cellular movements allowing cell-cell and/or cell-matrix interactions. Endothelial cells, on the contrary, developed both from drug-treated and from unincubated blastoderms, indicating that their commitment occurs before and independent of gastrulation and does not require DNA replication during gastrulation.

Adenosine↗

PubMed2004

Rb family proteins differentially regulate distinct cell lineages during epithelial development.

pRb, p107 and p130 are important regulators of cell cycle and have extensive overlapping functions; however, only Rb has been shown to be a bone fide tumor suppressor. Defining the overlapping versus distinct pocket protein functions is therefore an important step to understanding the unique role of Rb. Using lung as a model, the present studies demonstrate that pocket proteins are important not only in regulating cell cycle and survival but also in cell lineage specification. An inducible lung-specific Rb knockout strategy was used to demonstrate that Rb is specifically required for restricting neuroendocrine cell fate despite functional compensation for Rb deficiency in other cell types. Ablation of total Rb family function resulted in opposing effects in specification along distinct cell lineages, providing evidence that pocket proteins inhibit neuroendocrine cell fate while being required for differentiation in other cell types. These findings identify a novel role for pocket proteins in cell fate determination, and establish a unique cell lineage-specific function for Rb that explains, at least in part, why Rb and p16 are inactivated in phenotypically distinct carcinomas.

Animals↗

PubMed1984

Volume regulation in lymphoid leukemia cells and assignment of cell lineage.

Normal T lymphocytes readjust their volume after swelling in hypotonic medium, whereas B lymphocytes remain swollen. The difference between the two cell types appears to lie in the inability of B cells to increase their permeability to potassium in response to swelling. We have studied mononuclear cells from the bone marrow of 65 patients with lymphocytic leukemia, to determine whether the response to a hypotonic environment could be used to assign cell lineage. In contrast to leukemic cells of B-cell lineage (as in B-cell acute or chronic lymphocytic leukemia and non-T-cell, non-B-cell acute lymphocytic leukemia), T-cell-leukemia cells responded within five minutes to hypotonic swelling with an increase in potassium permeability and restoration toward isotonic volume. We conclude that the response to hypotonic shock may distinguish leukemic cells of T-cell origin from those derived from B-cell precursors and provides a simple, rapid, and reliable means for assigning cell lineage to lymphoid leukemia cells.

B-Lymphocytes↗

PubMed1995

Intrathymic T cell receptor (TcR) targeting in mice lacking CD4 or major histocompatibility complex (MHC) class II: rescue of CD4 T cell lineage without co-engagement of TcR/CD4 by MHC class II.

A critical step during intrathymic T cell development, termed positive selection, is associated with rescue of short-lived, immature thymocytes from programmed cell death, T cell lineage commitment, and induction of lineage-specific differentiation programs. T cell receptor (TcR)-major histocompatibility complex (MHC) interactions during positive selection can be closely mimicked by targeting TcR on immature thymocytes to cortical epithelial cells in situ via hybrid antibodies. Here, we show that antibody-mediated TcR signaling in mice deficient for CD4 or MHC class II expression induces polyclonal differentiation of the CD4 T cell lineage. Following a single TcR signal pulse in situ, a temporal sequence of phenotype changes can be discerned: CD69 up-regulation (< 1 day), CD8 down-regulation, TcR up-regulation (1-1.5 days) and down-regulation of the heat-stable antigen (1.5-2 days). Differentiation of phenotypically and functionally mature CD4 T cells in situ is attained within 3 days. Rescue of CD4 lineage T cells in the absence of TcR/CD4 co-engagement by MHC class II in this experimental system supports the stochastic/selective model of T cell lineage commitment.

Animals↗

PubMed2001

Lead alters the developmental profile of the galactolipid metabolic enzymes in cultured oligodendrocyte lineage cells.

Lead is a neurotoxicant that can cause myelin deficits. Galactolipids are expressed during differentiation of oligodendrocyte lineage cells and accumulate in myelin. To examine the impact of lead on oligodendroglial differentiation, galactolipid metabolism in cultured oligodendrocyte lineage cells exposed to the metal was studied. Oligodendrocyte progenitor cells obtained from newborn rat pups were exposed to 1 microM lead acetate for 24 h prior to maintenance of the cells in medium containing the metal salt for 0, 2, or 6 days of differentiation. Lead caused approximately 50% reduction in levels of the galactolipid biosynthetic transferases, UDP-galactose:ceramide galactosyltransferase and 3'-phosphoadenosine-5'-phosphosulfate:galactocerebroside sulfotransferase, as compared to sodium-treated controls, in cultures of oligodendrocyte lineage cells following 2 days of differentiation. The activities of the galactolipid catabolic hydrolases, galactocerebroside-beta-galactosidase and arylsulfatase A, were reduced by 20%. Following 6 days of differentiation, lead-exposed cells exhibited levels of all the enzymes, except for arylsulfatase A, similar to those of the control cells. These results are consistent with the lead-induced delay of oligodendrocyte differentiation, as evidenced by the emergence of stage-specific immunochemical markers and the observed change in the developmental activity profile of 2',3'-cyclic nucleotide 3'-phosphohydrolase. The activity of arylsulfatase A in lead-treated 6-day oligodendrocytes was significantly less than that found in control cultures. This effect is consistent with the lead-induced reduction of arylsulfatase A in human fibroblasts caused by mis-sorting the newly-synthesized enzyme. The perturbation of galactolipid metabolism by lead during developmental maturation of oligodendrocytes may represent a contributing mechanism for lead-induced neurotoxicity.

Animals↗

PubMed1978

Features of cell lineage in preimplantation mouse development.

The cell lineage of the mouse was studied from the 2-cell stage to the blastocyst. Lineage to the 8-cell stage was followed under the microscope. Each cell from the 2-cell stage divided to form two daughter cells which remained attached. Subsequently, these two daughters each produced two descendants; one of these descendants regularly lay deep in the structure of the embryo while the other was peripheral. Lineage to the blastocyst was followed by injecting oil drops into cells at the 8-cell stage, and then following the segregation of these drops into the inner cell mass and trophectoderm. Between the 8-cell stage and the blastocyst, the deep cells contributed more frequently to the inner cell mass than did the peripheral cells.

Animals↗

PubMed2000

Peroxisome proliferator activator receptor-gamma agonists and 15-deoxy-Delta(12,14)(12,14)-PGJ(2) induce apoptosis in normal and malignant B-lineage cells.

The research described herein evaluates the expression and functional significance of peroxisome proliferator activator receptor-gamma (PPAR-gamma) on B-lineage cells. Normal mouse B cells and a variety of B lymphoma cells reflective of stages of B cell differentiation (e.g., 70Z/3, CH31, WEHI-231, CH12, and J558) express PPAR-gamma mRNA and, by Western blot analysis, the 67-kDa PPAR-gamma protein. 15-Deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)), a PPAR-gamma agonist, has a dose-dependent antiproliferative and cytotoxic effect on normal and malignant B cells as shown by [(3)H]thymidine and 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide assays. Only PPAR-gamma agonists (thiazolidinediones), and not PPAR-alpha agonists, mimicked the effect of 15d-PGJ(2) on B-lineage cells, indicating that the mechanism by which 15d-PGJ(2) negatively affects B-lineage cells involves in part PPAR-gamma. The mechanism by which PPAR-gamma agonists induce cytotoxicity is via apoptosis, as shown by annexin V staining and as confirmed by DNA fragmentation detected using the TUNEL assay. Interestingly, addition of PGF(2alpha), which was not known to affect lymphocytes, dramatically attenuated the deleterious effects of PPAR-gamma agonists on B lymphomas. Surprisingly, 15d-PGJ(2) induced a massive increase in nuclear mitogen-activated protein kinase activation, and pretreatment with PGF(2alpha) blunted the mitogen-activated protein kinase activation. This is the first study evaluating PPAR-gamma expression and its significance on B lymphocytes. PPAR-gamma agonists may serve as a counterbalance to the stimulating effects of other PGs, namely PGE(2), which promotes B cell differentiation. Finally, the use of PGs, such as 15d-PGJ(2), and synthetic PPAR-gamma agonists to induce apoptosis in B-lineage cells may lead to the development of novel therapies for fatal B lymphomas.

Animals↗

PubMed1995

Cell lineage and patterns of migration in the developing cortex.

Knowledge of cell lineage in the cortex is important for understanding normal development as well as brain malformations. We studied cell lineage in rats by injecting a library of up to 3400 retroviruses, distinguishable by PCR analysis and encoding alkaline phosphatase, at E14-19. Histological analysis at P15 revealed normal cell morphology and allowed identification of about 80% of all labelled cells. PCR amplification of DNA tags allowed clonal analysis. Cortical cells labelled at E15 formed clustered or widespread clones with equal frequency. Clustered clones contained one to four cells within about 1 mm that had similar morphology and laminar location. However, 48% of cortical clones contained multiple cell types with widely different locations (2.1-6.7 mm; mean, 3.8 mm). Widespread clones contained two to four 'subunits' (one to five neurons each), spaced at apparent intervals of 2-3 mm, with each subunit morphologically indistinguishable from a clustered clone. Distinct subunits in the same clone usually differed in laminar location suggesting sequential formation. Clones labelled at E17 contained fewer neurons and up to two subunits. Clustered clones seem to be produced by stationary progenitors, whereas progenitors of clusters may themselves be produced by migratory, multipotential cells.

Animals↗

PubMed1996

Prostatic cell lineage markers: emergence of BCL2+ cells of human prostate cancer xenograft LuCaP 23 following castration.

A model of prostate cancer progression based on the expression pattern of informative genes in the human prostate cancer xenograft LuCaP 23.1 is presented. Apparently, there are at least 2 tumor cell populations of LuCaP 23.1, representing 2 different phenotypes. One is NSE (neuron-specific enolase)-positive and the other NSE-negative. NSE-positive tumors were recovered after hormone-independent growth in castrated mice. These hormone-independent tumors also expressed BCL2, a gene product shown to inhibit apoptosis. With NSE, BCL2 and PSA (prostate-specific antigen) as identifying markers, the model specifies a putative progression sequence of the prostate cancer cell types. We also show a proposed lineage relationship among the 3 principal normal cell types found in the prostatic epithelium.

Animals↗

PubMed1992

Surface markers, heavy chain sequences and B cell lineages.

A unifying theory of B cell development and lineage commitment is presented. There are two firmly established B lineages: cells which normally arise only from fetal sources and lack N insertions in their rearranged heavy chains; and N-containing cells which arise from adult bone marrow precursors (and perhaps from late fetal sources). Commitment to the expression of CD5 and the capacity for long-life (or self-renewal) are induced as a consequence of sIg cross-linking, typically by a repeating epitope, thymus independent type two antigen. Alternatively, activation resulting from cognate interaction with a helper T cell does not induce CD5 but results in lower expression of J11d. In this case activation occurs in the absence of sIg cross-linking. It is further proposed that differences in the Ig repertoire make it highly likely that fetal/neonatal, but not adult derived B cells will be induced to express CD5. The model offers a plausible explanation for the correlation of CD5 expression and natural autoantibody production by neonatal B cells. Possible sources of pathogenic autoantibody are discussed in the context of this model.

Animals↗

PubMed1990

Analysis of immunoglobulin and T-cell receptor gene rearrangements in human fetal bone marrow B lineage cells.

Fetal bone marrow B lineage cells representing multiple stages of B cell development were isolated by two-color cell sorting and analyzed for immunoglobulin H and T-cell receptor (TCR) gamma and delta gene rearrangements. Analysis of CD10+/surface mu- cells using a JH probe revealed a high frequency of rearrangements; some of these rearrangements used the 3' D region gene DQ52. Analysis of CD10+/surface mu- cells revealed no detectable TCR-gamma or -delta rearrangements, nor were TCR-delta rearrangements detected in CD10+/surface mu+ cells, despite the limited repertoire of these genes. These observations are surprising given the high frequency of TCR delta/gamma rearrangements in B cell precursor acute lymphoblastic leukemia, and identify a potential difference in patterns of gene rearrangement that distinguish normal and leukemic B cell precursors.

B-Lymphocytes↗

PubMed1996

An activated form of Notch influences the choice between CD4 and CD8 T cell lineages.

Notch is a transmembrane receptor that controls cell fate decisions in Drosophila and whose role in mammalian cell fate decisions is beginning to be explored. We are investigating the role of Notch in a well-studied mammalian cell fate decision: the choice between the CD8 and CD4 T cell lineages. Here we report that expression of an activated form of Notch1 in developing T cells of the mouse leads to both an increase in CD8 lineage T cells and a decrease in CD4 lineage T cells. Expression of activated Notch permits the development of mature CD8 lineage thymocytes even in the absence of class I major histocompatability complex (MHC) proteins, ligands that are normally required for the development of these cells. However, activated Notch is not sufficient to promote CD8 cell development when both class I and class II MHC are absent. These results implicate Notch as a participant in the CD4 versus CD8 lineage decision.

Animals↗

PubMed1990

Clonal analysis of the cell lineages in the male flower of maize.

The cell lineages in the male flower of maize were characterized using X-rays and transposable elements to produce clonal sectors differing in anthocyanin pigmentation. Less than 50% of the somatic tassel mutations (caused by reversion of unstable color mutations) that were visible on the anther wall were sexually transmitted by the male gametes, unless the sectors were larger than half the tassel circumference. This result is explained by showing that: (a) both the outer (LI) and inner (LII) lineages of the shoot apical meristem form a cell layer in the bilayered anther wall, and that anther pigmentation can be derived from either cell layer; and that (b) the male germ cells are derived almost exclusively from the LII. Therefore, while reversion events in either the LI or LII are visible on the anther, only the LII events are heritable. Reversion events that occur prior to the organization of the shoot apical meristem however, produce large (usually more than one-half tassel) sectors that include both the outer and inner lineages. In contrast to the high level of cell layer invasion previously reported during leaf development, during anther development less than 10(-3) cells in the LI invade the LII to form male gametes. The strong correlation between cell lineage and cell fate in the maize anther has implications for studies on plant evolution and the genetic improvement of cereals by DNA transformation.

Anthocyanins↗

PubMed1997

Cell-lineage and clonal-contribution map of the trochophore larva of Patella vulgata (mollusca).

Molluscan development is characterised by its extremely regular cleavage pattern. In numerous molluscs the fate of various early-cleavage stage blastomeres has been determined and fate maps have been constructed. On the basis of similarities between these fate maps, a generalised molluscan cell-lineage map has been constructed. Recently, the validity of this map has been challenged. In this study, the cell-lineage of the first-, second-, and third-quartet micromeres and third-generation macromeres of the equally-cleaving gastropod mollusc Patella vulgata was studied by fluorescent cell-lineage tracer injection followed by epifluorescence microscopy and confocal laser scanning microscopy. For the first time, a complete cell-lineage map, in the form of a clonal-contribution map of the trochophore, has been constructed with the use of fluorescent cell-lineage tracers. This map both agrees and differs in a number of respects with the generalised cell-lineage map of molluscs. The most important deviation is that the micromere 2d, formerly referred to as the first somatoblast, is not the only cell that forms the foot and shell gland in Patella.

Animals↗

PubMed2005

The role of p38 MAPK in rhinovirus-induced monocyte chemoattractant protein-1 production by monocytic-lineage cells.

Viral respiratory infections are a major cause of asthma exacerbations and can contribute to the pathogenesis of asthma. Major group human rhinovirus enters cells by binding to the cell surface molecule ICAM-1 that is present on epithelial and monocytic lineage cells. The focus of the resulting viral infection is in bronchial epithelia. However, previous studies of the cytokine dysregulation that follows rhinovirus infection have implicated monocytic lineage cells in establishing the inflammatory environment even though productive infection is not a result. We have determined that human alveolar macrophages and human peripheral blood monocytes release MCP-1 upon exposure to human rhinovirus 16 (HRV16). Indeed, we have found p38 MAPK activation in human alveolar macrophages within 15 min of exposure to HRV16, and this activation lasts up to 1 h. The targets of p38 MAPK activation include transcriptional activators of the MCP-1 promoter. The transcription factor ATF-2, a p38 MAPK substrate, is phosphorylated 45 min after HRV16 exposure. Furthermore, IkappaBalpha, the inhibitor of the transcription factor NF-kappaB, is degraded. Prevention of HRV16 binding was effective in blocking p38 MAPK activation, ATF-2 phosphorylation, and MCP-1 release. This is the first report of a relationship between HRV16 exposure, MCP-1 release and monocytic-lineage cells suggesting that MCP-1 plays a role in establishing the inflammatory microenvironment initiated in the human airway upon exposure to rhinovirus.

Activating Transcription Factor 2↗