scholarly journals Plasticity of Hepatic Cell Differentiation: Bipotential Adult Mouse Liver Clonal Cell Lines Competent to Differentiate In Vitro and In Vivo

Stem Cells ◽  
2006 ◽  
Vol 24 (9) ◽  
pp. 2098-2109 ◽  
Author(s):  
Catherine Fougère-Deschatrette ◽  
Tereza Imaizumi-Scherrer ◽  
Hélène Strick-Marchand ◽  
Serban Morosan ◽  
Pierre Charneau ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Cell Lines ◽  
Mouse Liver ◽  
Adult Mouse ◽  
Hepatic Cell ◽  
Clonal Cell ◽  
Clonal Cell Lines ◽  
Adult Mouse Liver

Vitamin D as Radiosensitizer: A Review in Cell Line -

2020 ◽  
Vol 10 (6) ◽  
pp. 315-324
Author(s):  
Fahmi Radityamurti ◽  
Fauzan Herdian ◽  
Tiara Bunga Mayang Permata ◽  
Handoko Handoko ◽  
Henry Kodrat ◽  
...  
Keyword(s):  
Vitamin D ◽  
Cell Differentiation ◽  
Cell Line ◽  
Cell Lines ◽  
Anticancer Agent ◽  
Medical Literature ◽  
In Vitro Studies ◽  
Anti Cancer

Introduction: Vitamin D has been shown to have anti-cancer properties such as antioxidants, anti-proliferative, and cell differentiation. The property of vitamin D as an anticancer agent triggers researchers to find out whether vitamin D is useful as a radiosensitizer. Multiple studies have been carried out on cell lines in various types of cancer, but the benefits of vitamin D as a radiosensitizer still controversial. This paperwork aims to investigate the utilization of Vitamin D3 (Calcitriol) as radiosensitizer in various cell line through literature review.Methods: A systematic search of available medical literature databases was performed on in-vitro studies with Vitamin D as a radiosensitizer in all types of cell lines. A total of 11 in-vitro studies were evaluated.Results: Nine studies in this review showed a significant effect of Vitamin D as a radiosensitizer agent by promoting cytotoxic autophagy, increasing apoptosis, inhibiting of cell survival and proliferation, promoting gene in ReIB inhibition, inducing senescene and necrosis. The two remaining studies showed no significant effect in the radiosensitizing mechanism of Vitamin D due to lack of evidence in-vitro settings.Conclusion: Vitamin D have anticancer property and can be used as a radiosensitizer by imploring various mechanism pathways in various cell lines. Further research especially in-vivo settings need to be evaluated.

Glutathione S-transferases in tracheobronchial epithelium

1995 ◽  
Vol 269 (4) ◽  
pp. L473-L481
Author(s):  
P. M. Reddy ◽  
C. P. Tu ◽  
R. Wu
Keyword(s):  
Cell Differentiation ◽  
Environmental Factors ◽  
Enzymatic Activity ◽  
Cell Lines ◽  
Mucous Cell ◽  
Collagen Gel ◽  
Bronchial Epithelium ◽  
High Level

The purpose of this study is to characterize glutathione S-transferase (GST) gene expression in airway epithelium both in vivo and in vitro. Immunohistochemical staining of nonhuman primate lungs of well-controlled healthy animals reveals the presence of alpha- and pi-class GST isoenzymes in ciliated bronchial epithelium. The stain of mu-GST antibody is either very low or absent in some of these monkey lungs. We observed that primary tracheobronchial epithelial (TBE) cells isolated from human and monkey pulmonary tissues maintain a relatively high level of GST enzymatic activity in culture, compared with various immortalized human TBE cell lines and other nonpulmonary cell lines. Northern blot analysis demonstrated the presence of mu-, pi-, and microsomal-GST messages but not the alpha-class message in cultures of primary TBE cells as well as in various human TBE cell lines. The expression of mu- and pi-class GST genes can be further regulated in culture by various environmental factors; however, most of these regulating factors are associated with TBE cell differentiation in culture. For instance, vitamin A treatment, which was shown to enhance mucous cell differentiation in vitro, stimulated the message levels of mu- and pi-class GST. Furthermore, plating cells on collagen gel substrata, which also enhanced mucous cell differentiation in culture, instead of plastic culture surface, enhanced total GST enzymatic activity by eightfold, and this enhancement is related to an increase in the expression of the pi-class GST gene. These results demonstrated that GST genes are differentially expressed and regulated by various environmental factors in primary TBE cells and various cell lines, and the regulation is correlated to the mucous cell differentiation in culture.

Hepcidin Inhibition by Modified Heparins without Anticoagulant Activity

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 483-483
Author(s):  
Maura Poli ◽  
Domenico Girelli ◽  
Annamaria Naggi ◽  
Natascia Campostrini ◽  
Dario Finazzi ◽  
...  
Keyword(s):  
Cell Lines ◽  
Conflicts Of Interest ◽  
Anticoagulant Activity ◽  
Hepatic Cell ◽  
Maximum Effect ◽  
Hepcidin Expression ◽  
Serum Hepcidin ◽  
Hepatic Cell Lines

Abstract Abstract 483 Background. There is an increasing interest in the development of pharmacological agents able to modulate hepcidin, the peptide hormone that critically regulates iron metabolism. In particular, hepcidin antagonist may have a therapeutic role in the anemia of chronic diseases, where hepcidin levels are often increased by pro-inflammatory cytokines. We previously demonstrated that heparin is a potent inhibitor of hepcidin expression in hepatic cell lines, probably by interfering with BMP/HJV/SMAD signalling, and that it was also effective in reducing hepcidin expression in mice (Poli M, Blood 2011; 117:997–1004). Since the therapeutic use of heparin for hepcidin modulation is hampered by its strong anticoagulant activity, we were interested in evaluating modified heparins without such activity. Methods. Heparins modified to inactivate the antithrombin binding site, with different molecular weight and degree of sulfation, were supplied to hepatic cell lines and mice to evaluate their potential modulation of hepcidin expression. We analysed their interference with the BMP/SMAD signalling, as well as serum hepcidin levels in mice by mass spectrometry. Results. Over 20 modified heparins were initially screened by evaluating their dose-dependent suppression of hepcidin expression before and after BMP induction. All of them showed a certain degree of anti-hepcidin activity, with two glycol-split molecules being as potent as classical unfractionated heparin. These two molecules suppressed BMP/SMAD signalling in HepG2 cells at pharmacological concentrations with maximum inhibition after 6 hours. In mice, treatments with 20 or 60 mg/Kg did not affect coagulation but strongly reduced liver pSMAD, hepcidin mRNA and serum hepcidin. Again, the maximum effect on liver hepcidin expression was observed 6 hours after the injection. This effect was observed also in conditions of high hepcidin caused by experimental inflammation or iron overload. Conclusions. Some non-anticoagulant heparins have strong anti-hepcidin activity both in vitro and in vivo, and may represent promising hepcidin antagonist with potential therapeutic applications. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Transformation of Tetrahymena thermophila with hypermethylated rRNA genes.

1988 ◽  
Vol 8 (4) ◽  
pp. 1664-1669 ◽  
Author(s):  
K M Karrer ◽  
M C Yao
Keyword(s):  
Cell Lines ◽  
Transformation Efficiency ◽  
Tetrahymena Thermophila ◽  
Host Cells ◽  
Rrna Genes ◽  
Major Constituent ◽  
Clonal Cell ◽  
Clonal Cell Lines

The extrachromosomal rRNA genes (rDNA) of Tetrahymena thermophila contain 0.4% N6-methyladenine. C3 strain rDNA was isolated, hypermethylated in vitro, and microinjected into B strain host cells. Clonal cell lines were established, and transformants were selected on the basis of resistance to paromomycin, conferred by the injected rDNA. The effects of methylation by three enzymes which methylate the sequence 5'-NAT-3', the dam, EcoRI, and ClaI methylases, were tested. Hypermethylation of the injected rDNA had no effect on transformation efficiency relative to mock-methylated controls. The injected C3 strain rDNA efficiently replaced host rDNA as the major constituent of the population of rDNA molecules. Hypermethylation of the injected DNA was not maintained through 20 to 25 cell generations.

scholarly journals β-Cell Differentiation from a Human Pancreatic Cell Line in Vitro and in Vivo

2001 ◽  
Vol 15 (3) ◽  
pp. 476-483 ◽  
Author(s):  
Dominique Dufayet de la Tour ◽  
Tanya Halvorsen ◽  
Carla Demeterco ◽  
Björn Tyrberg ◽  
Pamela Itkin-Ansari ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cell Differentiation ◽  
Cell Transplantation ◽  
Cell Lines ◽  
Β Cells ◽  
Β Cell ◽  
Cell Transplantation Therapy ◽  
Transplantation Therapy

Abstract Cell transplantation therapy for diabetes is limited by an inadequate supply of cells exhibiting glucose-responsive insulin secretion. To generate an unlimited supply of human β-cells, inducibly transformed pancreatic β-cell lines have been created by expression of dominant oncogenes. The cell lines grow indefinitely but lose differentiated function. Induction of β-cell differentiation was achieved by stimulating the signaling pathways downstream of the transcription factor PDX-1, cell-cell contact, and the glucagon-like peptide (GLP-1) receptor. Synergistic activation of those pathways resulted in differentiation into functional β-cells exhibiting glucose-responsive insulin secretion in vitro. Both oncogene-expressing and oncogene-deleted cells were transplanted into nude mice and found to exhibit glucose-responsive insulin secretion in vivo. The ability to grow unlimited quantities of human β-cells is a major step toward developing a cell transplantation therapy for diabetes.

276 PRODUCTION OF TRANSGENIC MINI-PIG CELL LINES EXPRESSING HUMAN CYTOMEGALOVIRUS US2

2007 ◽  
Vol 19 (1) ◽  
pp. 254
Author(s):  
K. W. Park ◽  
J. Y. Yoo ◽  
K. M. Choi ◽  
S. P. Hong ◽  
G. S. Han ◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Cytomegalovirus ◽  
Recombinant Expression ◽  
Class I ◽  
Class I Mhc ◽  
Specific Lysis ◽  
Clonal Cell ◽  
Fetal Fibroblasts ◽  
Clonal Cell Lines

Xenotransplantation has the potential to resolve the chronic shortage of donor organs if immunological barriers can be overcome. In particular, the initial type of rejection following xenotransplantation is acute cellular rejection by host CD8+ cytotoxic T lymphocyte (CTL) cells that react to the donor class I major histocompatibility complex (MHC). The human cytomegalovirus (HCMV) glycoprotein US2 specifically targets class I MHC heavy chains for dislocation from the endoplasmic reticulum (ER) membrane to the cytosol, where they are degraded by the proteasome. In this study, the recombinant expression vector pCX-US2 was stably transfected into mini-pig fetal fibroblasts by lipofection. The integration of US2 into the host genome was confirmed by PCR and Southern blot assay. The reduction of swine leukocyte antigen class I (SLA-I, MHC protein class I) by US2 was detected by flow cytometry analysis (FACS). FACS analysis of US2 clonal cell lines demonstrated substantial reductions in SLA surface expression. The decrease in the level of class I MHC expression for US2 clonal cell lines ranged from 22 to 34% relative to the non-transfected control. US2 clonal cell lines were also tested to determine if the resulting reduction in cell surface SLA would reduce in vitro cytotoxicity by CTL. The US2 clonal cell line demonstrated 5- to 6-fold reduction of specific lysis by primed CD8+ CTL. In conclusion, US2 can directly protect pig clonal cell lines from human CTL cells. These results indicate that the expression of US2 in pig cells may provide a new approach toward overcoming CTL-mediated immunity to xenotransplantation. This work was supported by the National Livestock Research Institute (6132-211-303-1).

Gene Expression Studies Reveal a Potential Mechanism of Glivec Resistance in Patients with Ph+ ALL Treated.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4374-4374
Author(s):  
To Ha Loi ◽  
David D.F. Ma
Keyword(s):  
Gene Expression ◽  
Cell Differentiation ◽  
B Cell ◽  
Cell Lines ◽  
Unexpected Finding ◽  
B Cell Differentiation ◽  
Down Regulation ◽  
Blast Cells

Abstract In Ph+ ALL, patients respond to Glivec but nearly always relapse due to acquired resistance. The biological processes associated with Glivec resistance in Ph+ ALL are yet to be fully elucidated. The aim of this study is to use microarray and Q-PCR technology to dissect changes in signaling pathways of blast cells in Ph+ ALL patients treated with Glivec. Peripheral blood (PB) samples were taken before treatment and on consecutive days after administration of Glivec from two Ph+, c-ALLA+ and CD19+ ALL patients. Blast cells were isolated and their gene expression assayed using 19K cDNA microarrays. Over 400 differentially expressed genes were identified with at least a 1.5-fold up- or down-regulation in treated cells compared to cells collected pre-treatment. Based on these gene expression results, three main gene ontology groups were further evaluated: Apoptosis, Proliferation and B cell differentiation. The up-regulation of Bim and Bcl-6, and down regulation of Cyclin D2, confirms the induction of apoptosis via the FOXO3a pathway in cells treated with Glivec in vivo. Interestingly, both the proliferation genes, Tcl1-A and PKCe, and B cell differentiation associated genes, including CD79a, ETS1 and a cohort of IGH and Igl and k genes, were up-regulated during therapy. These gene expression changes observed in vivo were confirmed by Q-PCR in the Ph+ cell lines K562 (derived from CML blast crisis) and SUP-B15 (derived from ALL) treated with Glivec. The unexpected finding of increased expression of pro-proliferative genes and B cell differentiation genes by microarray revealed potential links with early B cell development and B cell receptor (BCR) signaling. Evidence for apoptosis and proliferation of Ph+ cell lines treated with Glivec were then examined by FACs. After 5 days of treatment with Glivec, 90% of K562 and 50% SUP-B15 cells underwent apoptosis. Furthermore, cell cycle analysis revealed the existence of a population of cells in G2 phase even after 6 days of Glivec treatment in SUP-B15 but not K562 cells, thus providing evidence of a population of cells undergoing proliferation during Glivec treatment in vitro. In summary, our in vivo observations supported by in vitro experiments suggest that Glivec induces the majority of Ph+ ALL blasts to undergo apoptosis. However, as treatment is prolonged, a population of ALL cells escapes death and undergoes proliferation and differentiation. We hypothesise that Glivec induced differentiation and proliferation of Ph+ cells may result in the clonal enrichment of cells resistant to Glivec.

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