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1
Hannes, Tobias, Marie Wolff, Michael Xavier Doss, Kurt Pfannkuche, Moritz Haustein, Jochen Müller-Ehmsen, Agapios Sachinidis, Jürgen Hescheler, Markus Khalil, and Marcel Halbach. "Electrophysiological Characteristics of Embryonic Stem Cell-Derived Cardiomyocytes are Cell Line-Dependent." Cellular Physiology and Biochemistry 35, no. 1 (2015): 305–14. http://dx.doi.org/10.1159/000369697.
Повний текст джерелаАнотація:
Background: Modelling of cardiac development, physiology and pharmacology by differentiation of embryonic stem cells (ESCs) requires comparability of cardiac differentiation between different ESC lines. To investigate whether the outcome of cardiac differentiation is consistent between different ESC lines, we compared electrophysiological properties of ESC-derived cardiomyocytes (ESC-CMs) of different murine ESC lines. Methods: Two wild-type (D3 and R1) and two transgenic ESC lines (D3/aPIG44 and CGR8/AMPIGX-7) were differentiated under identical culture conditions. The transgenic cell lines expressed enhanced green fluorescent protein (eGFP) and puromycin-N-acetyltransferase under control of the cardiac specific α-myosin heavy chain (αMHC) promoter. Action potentials (APs) were recorded using sharp electrodes and multielectrode arrays in beating clusters of ESC-CMs. Results: Spontaneous AP frequency and AP duration (APD) as well as maximal upstroke velocity differed markedly between unpurified CMs of the four ESC lines. APD heterogeneity was negligible in D3/aPIG44, moderate in D3 and R1 and extensive in CGR8/AMPIGX-7. Interspike intervals calculated from long-term recordings showed a high degree of variability within and between recordings in CGR8/AMPIGX-7, but not in D3/aPIG44. Purification of the αMHC+ population by puromycin treatment posed only minor changes to APD in D3/aPIG44, but significantly shortened APD in CGR8/AMPIGX-7. Conclusion: Electrophysiological properties of ESC-CMs are strongly cell line-dependent and can be influenced by purification of cardiomyocytes by antibiotic selection. Thus, conclusions on cardiac development, physiology and pharmacology derived from single stem cell lines have to be interpreted carefully.
2
Lasky, SR, MR Posner, K. Iwata, A. Santos-Moore, A. Yen, V. Samuel, J. Clark, and AL Maizel. "Characterization of a vitamin D3-resistant human chronic myelogenous leukemia cell line." Blood 84, no. 12 (December 15, 1994): 4283–94. http://dx.doi.org/10.1182/blood.v84.12.4283.bloodjournal84124283.
Повний текст джерелаАнотація:
A variant of the chronic myelogenous leukemia cell line, RWLeu-4, that is resistant to the antiproliferative effects of vitamin D3 was established. Although RWLeu-4 proliferation is inhibited by 1 nmol/L vitamin D3, the resistant cells (JMRD3) continue to proliferate in the presence of 100 nmol/L vitamin D3. Both cells express similar patterns of differentiation-specific antigens after treatment with vitamin D3, and both express the retinoblastoma gene product (p110Rb). Vitamin D3 treatment of the sensitive RWLeu-4 cells decreased the level of the p110Rb protein, as well as its phosphorylation. In contrast, vitamin D3 treatment of JMRD3 had no effect on p110Rb expression or phosphorylation. Both RWLeu-4 and JMRD3 express similar vitamin D3 receptors and vitamin D3-inducible enzyme activities. Differences were detected in the DNA binding characteristics of the vitamin D3 receptors as determined by electrophoretic mobility shift studies. However, sequence analysis of the DNA-binding domain and immunoblot analysis showed no differences in the receptors. We conclude that some process subsequent to vitamin D3 receptor activation is altered in JMRD3 that partially separates vitamin D3-induced inhibition of proliferation from the induction of differentiation.
3
Feigelstock, Dino A., Peter Thompson, and Gerardo G. Kaplan. "Growth of Hepatitis A Virus in a Mouse Liver Cell Line." Journal of Virology 79, no. 5 (March 1, 2005): 2950–55. http://dx.doi.org/10.1128/jvi.79.5.2950-2955.2005.
Повний текст джерелаАнотація:
ABSTRACT Hepatitis A virus (HAV) has been adapted to grow efficiently in primate and some nonprimate cell lines but not in cells of murine origin. To understand the inability of the virus to grow in mouse cells, we studied the replication of HAV in immortalized and nontransformed MMH-D3 mouse liver cells, which require growth factors and collagen to maintain their phenotype. HAV grew in MMH-D3 cells transfected with virion RNA but not in those infected with viral particles, indicating a cell entry block for HAV. However, MMH-D3 cells cultured under suboptimal conditions in the absence of growth factors acquired susceptibility to HAV infection. Serial passages of the virus in MMH-D3 cells under suboptimal growth conditions resulted in the selection of HAV variants that grew efficiently in MMH-D3 cells cultured under both optimal and suboptimal conditions. Nucleotide sequence analysis of the MMH-D3 cell-adapted HAV revealed that N1237D and D2132G substitutions were present in the capsid regions of six viral clones. These two mutations are most likely located on the surface of the virion and may play a role in the entry of HAV into the mouse liver cells. Our results demonstrate that mouse hepatocyte-like cells code for all factors required for the efficient growth of HAV in cell culture.
4
Kester, Monique H. A., George G. J. M. Kuiper, Rogier Versteeg, and Theo J. Visser. "Regulation of Type III Iodothyronine Deiodinase Expression in Human Cell Lines." Endocrinology 147, no. 12 (December 1, 2006): 5845–54. http://dx.doi.org/10.1210/en.2006-0590.
Повний текст джерелаАнотація:
Type I iodothyronine deiodinase (D1) and type II iodothyronine deiodinase (D2) catalyze the activation of the prohormone T4 to the active hormone T3; type III iodothyronine deiodinase (D3) catalyzes the inactivation of T4 and T3. D3 is highly expressed in brain, placenta, pregnant uterus, and fetal tissues and plays an important role in regulating thyroid hormone bioavailability during fetal development. We examined the activity of the different deiodinases in human cell lines and investigated the regulation of D3 activity and mRNA expression in these cell lines, as well as its possible coexpression with neighboring genes Dlk1 and Dio3os, which may also be especially important during development. D1 activity and mRNA were only found in HepG2 hepatocarcinoma cells, and D2 activity was observed in none of the cell lines. D3 activity and mRNA was found in ECC-1 endometrium carcinoma cells, MCF-7 mammacarcinoma cells, WRL-68 embryonic liver cells, and SH-SY5Y neuroblastoma cells, but not in the HepG2 hepatocarcinoma cell line or in any choriocarcinoma or astrocytoma cell line. We demonstrated that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate increased D3 activity 2- to 9-fold in ECC-1, MCF-7, WRL-68, and SH-SY5Y cells. Estradiol increased D3 activity 3-fold in ECC-1, but not in any other cells. Dexamethasone decreased D3 activity in WRL-68 cells only in the absence of fetal calf serum. Incubation with retinoids increased D3 activity 2- to 3-fold in ECC-1, WRL-68, and MCF-7 cells but decreased D3 activity in SH-SY5Y cells. D3 expression in the different cells was not affected by cAMP or thyroid hormone. Interestingly, D3 mRNA expression in the different cell lines strongly correlated with Dio3os mRNA expression and in a large set of neuroblastoma cell lines also with Dlk1 expression. In conclusion, we identified different human D3-expressing cell lines, in which the regulation of D3 expression is cell type-specific. Our data suggest that estradiol may be one of the factors contributing to the induction of D3 activity in the pregnant uterus and that in addition to gene-specific regulatory elements, more distant common regulatory elements also may be involved in the regulation of D3 expression.
5
Ravid, Amiram, Noa Rapaport, Assaf Issachar, Arie Erman, Larisa Bachmetov, Ran Tur-Kaspa, and Romy Zemel. "25-Hydroxyvitamin D Inhibits Hepatitis C Virus Production in Hepatocellular Carcinoma Cell Line by a Vitamin D Receptor-Independent Mechanism." International Journal of Molecular Sciences 20, no. 9 (May 13, 2019): 2367. http://dx.doi.org/10.3390/ijms20092367.
Повний текст джерелаАнотація:
Previously, we have reported that the active vitamin D metabolite, calcitriol and vitamin D3 (cholecalciferol), both remarkably inhibit hepatitis C virus production. The mechanism by which vitamin D3 exerts its effect is puzzling due to the low levels of calcitriol produced in vitamin D3-treated Huh7.5 cells. In this study, we aimed to explore the mechanism of vitamin D3 anti-hepatitis C virus effect. We show that vitamin D3 activity is not mediated by its metabolic conversion to calcitriol, but may be due to its primary metabolic product 25(OH)D3. This is inferred from the findings that 25(OH)D3 could inhibit hepatitis C virus production in our system, and that adequate concentrations needed to exert this effect are produced in Huh7.5 cells treated with vitamin D3. Using the CRISPR-Cas9 editing technology to knockout the vitamin D receptor, we found that the antiviral activity of vitamin D3 and 25(OH)D3 was not impaired in the vitamin D receptor knockout cells. This result indicates that 25(OH)D3 anti-hepatitis C virus effect is exerted by a vitamin D receptor-independent mode of action. The possibility that vitamin D3 and 25(OH)D3, being 3β-hydroxysteroids, affect hepatitis C virus production by direct inhibition of the Hedgehog pathway in a vitamin D receptor-independent manner was ruled out. Taken together, this study proposes a novel mode of action for the anti-hepatitis C virus activity of vitamin D3 that is mediated by 25(OH)D3 in a vitamin D receptor-independent mechanism.
6
Warrington, R. J., W. J. Rutherford, S. K. Wong, J. M. Cook, and E. S. Rector. "Low molecular weight B cell growth factor-responsive cloned human B cell lines. I. Phenotypic differences and lack of requirement for CD23 (Fc epsilon RII)." Journal of Immunology 143, no. 8 (October 15, 1989): 2546–52. http://dx.doi.org/10.4049/jimmunol.143.8.2546.
Повний текст джерелаАнотація:
Abstract The EBV-transformed B cell line JR-2 proliferates in response to partially purified preparations of low m.w. B cell growth factor (LMW-BCGF). Two clones of JR-2 were generated that retained this LMW-BCGF responsiveness, exhibiting similar dose/response characteristics but differing phenotypically. The B10 clone grows as single, discrete, small round cells, whereas D3 grows in aggregates. The clones also differ in the expression of cell surface Ag, D3 being weakly DR+ and strongly CD23+, whereas B10 lacks these Ag. The CD23 on D3 cells binds IgE. Both clones are T9+, 4F2+, B1-, B2- and CALLA-. D3 expresses surface IgG and differentiates in the presence of LMW-BCGF, to secrete IgG. B10 lacks surface and cytoplasmic Ig and fails to differentiate in response to LMW-BCGF. CD23 cannot be induced on B10 by incubation with either LMW-BCGF or IL-4. B10 does not shed CD23 and shed CD23 is not a growth factor for either cloned line. Expression of CD23 on D3 cells is not affected by preincubation with LMW-BCGF. Neither B10 or D3 cells respond to rIL-1, rIL-2, rIL-4, rIL-6, rTNF-alpha/beta, rIFN-gamma, or to high m.w. BCGF (Namalwa), alone or in combination. Both clones absorb BCGF activity and crossover absorptions indicate that the clones remove growth factors required by each other. D3 and B10 both appear therefore to respond selectively to LMW-BCGF. These data suggest that the loss of CD23 from a cloned derivative of the cell line JR-2, although accompanied by considerable phenotypic change, is not associated with the disappearance of LMW-BCGF responsiveness, indicating that CD23 is not the essential receptor for LMW-BCGF.
7
Narvaez, C. J., K. Vanweelden, I. Byrne, and J. Welsh. "Characterization of a vitamin D3-resistant MCF-7 cell line." Endocrinology 137, no. 2 (February 1996): 400–409. http://dx.doi.org/10.1210/endo.137.2.8593782.
Повний текст джерела
8
Quélo, I., and P. Jurdic. "Vitamin D3 regulated CAII gene in a macrophage cell line." Bone 17, no. 6 (December 1995): 584. http://dx.doi.org/10.1016/8756-3282(96)87893-8.
Повний текст джерела
9
Bar-Shavit, Zvi, Ronald L. Horst, Jean C. Chappel, F. Patrick Ross, Richard W. Gray, and Steven L. Teitelbaum. "25-Hydroxyvitamin D3 metabolism in a human leukemia cell line." Calcified Tissue International 39, no. 5 (September 1986): 328–33. http://dx.doi.org/10.1007/bf02555200.
Повний текст джерела
10
Koehler, M., R. Goorha, GR Kitchingman, GD Ayers, and J. Jr Mirro. "A monoclonal antibody to a novel surface antigen, MKW, blocks the antiproliferative and differentiation effects of granulocyte- macrophagecolony-stimulating factor and vitamin D3." Blood 80, no. 2 (July 15, 1992): 367–73. http://dx.doi.org/10.1182/blood.v80.2.367.bloodjournal802367.
Повний текст джерелаАнотація:
A monoclonal antibody (MoAb) recognizes a novel 52-Kd cell protein (MKW) that is expressed on cells of the normal myelocytic and monocytic lineage, a subset of B cells, and the U937 cell line. Using the U937 cell line as a model, the MoAb (anti-MKW) was examined for its ability to inhibit the effects of differentiation-inducing factors. In the U937 cell line, recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) inhibits cell proliferation, 12-O- tetradecanoylphorbol-13-acetate (TPA) inhibits proliferation and induces the early differentiation antigen CD11b, and vitamin D3 inhibits proliferation and induces both CD11b and the late differentiation antigen CD14. The antiproliferative and differentiation effects of rhGM-CSF and vitamin D3 on U937 cells were inhibited by the anti-MKW MoAb. Similar effects were seen when anti-MKW antibody was added 30 minutes before or 2 hours after rhGM-CSF or vitamin D3, suggesting that its effects are not mediated by blocking or binding to the receptors for these growth factors. The anti-MKW MoAb had no effect on TPA-induced differentiation in U937 cells, indicating that TPA exerts its effects through a pathway different from rhGM-CSF and vitamin D3. These results suggest that the MKW antigen is important in controlling the proliferation and differentiation of monocytic cells.
11
Baudet, Christel, Guillemette Chevalier, Agn�s Chassevent, C�cile Canova, Robert Filmon, Francis Larra, Philippe Brachet, and Didier Wion. "1,25-Dihydroxyvitamin D3 induces programmed cell death in a rat glioma cell line." Journal of Neuroscience Research 46, no. 5 (December 1, 1996): 540–50. http://dx.doi.org/10.1002/(sici)1097-4547(19961201)46:5<540::aid-jnr3>3.0.co;2-j.
Повний текст джерела
12
Weiler, Sarah R., John M. Gooya, Mariaestela Ortiz, Schickwann Tsai, Steven J. Collins, and Jonathan R. Keller. "D3: A Gene Induced During Myeloid Cell Differentiation of Linlo c-Kit+ Sca-1+ Progenitor Cells." Blood 93, no. 2 (January 15, 1999): 527–36. http://dx.doi.org/10.1182/blood.v93.2.527.
Повний текст джерелаАнотація:
Abstract In an effort to characterize molecular events contributing to lineage commitment and terminal differentiation of stem/progenitor cells, we have used differential display reverse transcription polymerase chain reaction (DDRT-PCR) and cell lines blocked at two distinct stages of differentiation. The cell lines used were EML, which is representative of normal multipotential primitive progenitors (Sca-1+, CD34+, c-Kit+, Thy-1+) able to differentiate into erythroid, myeloid, and B-lymphoid cells in vitro, and MPRO, which is a more committed progenitor cell line, with characteristics of promyelocytes able to differentiate into granulocytes. One clone isolated by this approach was expressed in MPRO but not in EML cells and contained sequence identical to the 3′ untranslated region of D3, a gene cloned from activated peritoneal macrophages of unknown function. We have observed a novel pattern of D3 gene expression and found that D3 is induced in EML cells under conditions that promote myeloid cell differentiation (interleukin-3 [IL-3], stem cell factor [SCF], and all-trans-retinoic acid [atRA]) starting at 2 days, corresponding to the appearance of promyelocytes. D3 RNA expression reached a maximum after 5 days, corresponding to the appearance of neutrophilic granulocytes and macrophages, and decreased by day 6 with increased numbers of differentiated neutrophils and macrophages in vitro. Induction of D3 RNA in EML was dependent on IL-3 and was not induced in response to SCF or atRA alone or SCF in combination with 15 other hematopoietic growth factors (HGF) tested. Similarly, D3 was not expressed in the normal bone marrow cell (BMC) counterpart of EML cells, Linlo c-Kit+Sca-1+ progenitor cells. D3 RNA expression was induced in these cells when cultured for 7 days in IL-3 plus SCF. A comparison of the expression of D3 RNA in cell lines and normal BMC populations demonstrated that D3 is induced during macrophage and granulocyte differentiation and suggests a potential physiological role for D3 in normal myeloid differentiation.
13
Weiler, Sarah R., John M. Gooya, Mariaestela Ortiz, Schickwann Tsai, Steven J. Collins, and Jonathan R. Keller. "D3: A Gene Induced During Myeloid Cell Differentiation of Linlo c-Kit+ Sca-1+ Progenitor Cells." Blood 93, no. 2 (January 15, 1999): 527–36. http://dx.doi.org/10.1182/blood.v93.2.527.402k32_527_536.
Повний текст джерелаАнотація:
In an effort to characterize molecular events contributing to lineage commitment and terminal differentiation of stem/progenitor cells, we have used differential display reverse transcription polymerase chain reaction (DDRT-PCR) and cell lines blocked at two distinct stages of differentiation. The cell lines used were EML, which is representative of normal multipotential primitive progenitors (Sca-1+, CD34+, c-Kit+, Thy-1+) able to differentiate into erythroid, myeloid, and B-lymphoid cells in vitro, and MPRO, which is a more committed progenitor cell line, with characteristics of promyelocytes able to differentiate into granulocytes. One clone isolated by this approach was expressed in MPRO but not in EML cells and contained sequence identical to the 3′ untranslated region of D3, a gene cloned from activated peritoneal macrophages of unknown function. We have observed a novel pattern of D3 gene expression and found that D3 is induced in EML cells under conditions that promote myeloid cell differentiation (interleukin-3 [IL-3], stem cell factor [SCF], and all-trans-retinoic acid [atRA]) starting at 2 days, corresponding to the appearance of promyelocytes. D3 RNA expression reached a maximum after 5 days, corresponding to the appearance of neutrophilic granulocytes and macrophages, and decreased by day 6 with increased numbers of differentiated neutrophils and macrophages in vitro. Induction of D3 RNA in EML was dependent on IL-3 and was not induced in response to SCF or atRA alone or SCF in combination with 15 other hematopoietic growth factors (HGF) tested. Similarly, D3 was not expressed in the normal bone marrow cell (BMC) counterpart of EML cells, Linlo c-Kit+Sca-1+ progenitor cells. D3 RNA expression was induced in these cells when cultured for 7 days in IL-3 plus SCF. A comparison of the expression of D3 RNA in cell lines and normal BMC populations demonstrated that D3 is induced during macrophage and granulocyte differentiation and suggests a potential physiological role for D3 in normal myeloid differentiation.
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Stuart, August, Sara Shimko, and Elliot M. Epner. "Crosstalk Between Cyclins D1 and D3 in Mantle Cell Level At the Transcriptional and Postranscriptional Levels." Blood 118, no. 21 (November 18, 2011): 1373. http://dx.doi.org/10.1182/blood.v118.21.1373.1373.
Повний текст джерелаАнотація:
Abstract Abstract 1373 Cyclin D1 (CCND1) expression is deregulated epigenetically in mantle cell lymphoma by the t(11;14) chromosome translocation. We have investigated the phenomenon of cyclin D1 mediated oncogene addiction in mantle cell lymphoma (MCL) and multiple myeloma (MM) cell lines. Gene targeting methods were utilized to generate Cyclin D1(-) MCL and MM cell lines. These cell lines did not make any detectable cyclin D1 mRNA and protein. These cells lines had shorter doubling times in vitro than their cyclin D1(+) counterparts and were also more chemoresistant in vitro and more tumorigenic in immunodeficient mice. Cyclin D3 mRNA and protein levels were increased dramatically. Q-RTPCR analysis showed a 17 fold increase in the mRNA of cyclin D3. The half-life of cyclin D3 protein was also significantly prolonged, from 20 minutes in wild type cells to 5 hours in mutant cyclin. Knockdown of cyclin D3 dramatically inhibited cell growth and caused apoptosis in the cyclin D1(-) but not in the t(11;14) cyclin D1 positive parental cells. Compensation and crosstalk between the cyclin D1 and D3 genes in MCL and MM cells were shown both in vitro and in vivo. Thus, the addiction to cyclin D1 in MCL and MM cells can be substituted by cyclin D3. Therapies that can target both cyclins D1 and D3 posttranscriptionally such as curcumin in combination with bortezomib were investigated in vitro in MCL cells. Combination treatment of MCL and MM cell lines with these agents produce significant downregulation of the protein levels of cyclins D1 and D3, even in cyclin D1(-) cell lines containing a extremely stable cyclin D3 protein. In addition, we have shown that iron chelators such as desferoxamine can turn off cyclin D1 transcription and cause apoptosis of MCL cells in vitro. Published work from several laboratories has described cyclin dependent kinase (Cdk) independent DNA binding activity for cyclin D1. Evidence that cyclin D1 and D3 might be involved in the pathogenesis of MCL in a cdk independent manner was observed. We confirmed that cyclin D1 is a DNA binding protein and demonstrated by chromatin immuprecipitation assays that it binds to the endogenous cyclin D3 gene promoter both in a MCL cell line and in cells from leukemic MCL patients. The binding site corresponds to a published E2F binding site upstream of exon 2, which regulates two cyclin D3 transcript variants. We have also identified several potential targets of cyclin D1 regulation based on published cyclin D1 microarray experiments, several of which exhibit promoter- enrichment following cyclin D1 CHIP: GSK3b, ID3, and ANSN. Thus, cyclin D1 is a potential repressor of cyclin D3 expression by direct binding to the cyclin D3 promoter. These data demonstrate crosstalk between cyclin D1 and D3 at both the transcriptional and post transcriptional levels. Furthermore, we demonstrate for the first time that cyclin D1 binds to the cyclin D3 promoter and potentially can mediate repression of cyclin D3 mRNA transcription. Deletion of cyclin D1 in an MCL cell line results in significant upregulation cyclin D3 mRNA and protein levels and a dramatic increase in the half life of cyclin D3 in cyclin D1 null cells. Previously reported data using knockdown and antisense technologies in MCL cell lines would be unable to appreciate these observations because of residual cyclin D1 mRNA and protein levels. Agents such as bortezomib and curcumin that downregulate cyclin D1 protein levels and iron chelating agents that downregulate cyclin D1 RNA levels may be useful agents in combination treatment of MCL and MM.Figure 1:CHIP assay of cyclin D1 binding to the E2F binding site within the Cyclin D3 (CCND3) gene promoter in vitro and in vivo. Antibodies used include pan-H3 (Cell Signal #9715), Cyclin D1 (Abcam ab16663) and Normal Rabbit IgG (rb; Santa Cruz).Figure 1:. CHIP assay of cyclin D1 binding to the E2F binding site within the Cyclin D3 (CCND3) gene promoter in vitro and in vivo. Antibodies used include pan-H3 (Cell Signal #9715), Cyclin D1 (Abcam ab16663) and Normal Rabbit IgG (rb; Santa Cruz). Disclosures: Epner: Merck: Consultancy, Honoraria, Speakers Bureau; Novartis: Speakers Bureau; Millenium: Speakers Bureau; Allos: Speakers Bureau; Enzon: Speakers Bureau; GSK: Speakers Bureau.
15
Valtieri, M., G. Boccoli, U. Testa, C. Barletta, and C. Peschle. "Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF." Blood 77, no. 8 (April 15, 1991): 1804–12. http://dx.doi.org/10.1182/blood.v77.8.1804.1804.
Повний текст джерелаАнотація:
Abstract The human AML-193 cell line requires exogenous granulocyte-monocyte colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3) for growth in liquid or semisolid medium. However, these CSFs do not stimulate the differentiation of the cell line. We show that addition of all-trans retinoic acid (RA) or 1,25 dihydroxyvitamin D3 (D3) induces AML-193 cells to differentiate into the granulocytic or monocytic lineage, respectively. On the other hand, addition of either G- or M-CSF alone exerts virtually no differentiative effect. Terminal granulocytic or monocytic differentiation was observed when AML-193 cells were treated with RA and G-CSF, or D3 and M-CSF, respectively, as evaluated by cell morphology, analysis of surface antigens, and phagocytic functions. These positive interactions indicate that the differentiating activity of G- and M-CSF on leukemic cells may be unmasked by preliminary treatment with RA and D3, respectively, ie, the physiologic inducers override the leukemic differentiation blockade and CFSs exert their differentiative activity on the unblocked leukemic cells. These preliminary observations on a single cell line may pave the way for the designing of clinical protocols combining physiologic inducer(s) and hematopoietic growth factor(s) in the treatment of acute leukemia.
16
Valtieri, M., G. Boccoli, U. Testa, C. Barletta, and C. Peschle. "Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF." Blood 77, no. 8 (April 15, 1991): 1804–12. http://dx.doi.org/10.1182/blood.v77.8.1804.bloodjournal7781804.
Повний текст джерелаАнотація:
The human AML-193 cell line requires exogenous granulocyte-monocyte colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3) for growth in liquid or semisolid medium. However, these CSFs do not stimulate the differentiation of the cell line. We show that addition of all-trans retinoic acid (RA) or 1,25 dihydroxyvitamin D3 (D3) induces AML-193 cells to differentiate into the granulocytic or monocytic lineage, respectively. On the other hand, addition of either G- or M-CSF alone exerts virtually no differentiative effect. Terminal granulocytic or monocytic differentiation was observed when AML-193 cells were treated with RA and G-CSF, or D3 and M-CSF, respectively, as evaluated by cell morphology, analysis of surface antigens, and phagocytic functions. These positive interactions indicate that the differentiating activity of G- and M-CSF on leukemic cells may be unmasked by preliminary treatment with RA and D3, respectively, ie, the physiologic inducers override the leukemic differentiation blockade and CFSs exert their differentiative activity on the unblocked leukemic cells. These preliminary observations on a single cell line may pave the way for the designing of clinical protocols combining physiologic inducer(s) and hematopoietic growth factor(s) in the treatment of acute leukemia.
17
Chanan-Khan, Asher Alban, Michelle Romano, Paula Pera, Noreen Ersing, Josephia Muindi, Donald L. Trump, and Candace Johnson. "Antiproliferative and Proapoptotic Effect of Vitamin D in Bortezomib (B) Resistant Human Myeloma Cell Line (HMCL)." Blood 108, no. 11 (November 16, 2006): 5074. http://dx.doi.org/10.1182/blood.v108.11.5074.5074.
Повний текст джерелаАнотація:
Abstract -Introduction: B is a proteasome inhibitor approved for treatment of multiple myeloma (MM) patients. Despite initial clinical efficacy all patients eventually become resistant to bortezomib and die of progressive disease. Development of newer agents with novel antitumor mechanisms is thus warranted. In vitro antiproliferative and proapoptotic effects of vitamin D are reported in various tumor models including MM. This is mediated through vitamin D receptor (VDR) which is also expressed on MM cells. Effect of calcitriol (D3) or its analog paricalcitol (D2) in HMCL resistant to B have not been previously examined. We investigated the antitumor potential of D3 and D2 in HMCL sensitive or resistant to B. Method & Results: HMCL sensitive (OPM-2) or resistant to B (OPM-2/BR) were treated with various concentration of D2 or D3. Significant growth inhibition and induction of apoptosis was noted with D2 and D3 that was maximal at 3 days (p<0.01). This antitumor response was noted despite resistance to B. Treatment of MM cells with vitamin D (D2 or D3) was associated with a loss of full-length PARP, decrease in p21 and induction of p27. Levels of the pro-survival molecules P-Akt and P-Erk were also reduced while total Akt and Erk remain unchanged. Conclusion: We demonstrate that the antiproliferative and proapoptotitc effect of vitamin D in HMCL are mediated through interruption of the Akt pathway and were independent of resistance to B. We have initiated a phase I clinical trial to investigate the clinical utility of paricalcitol in relapsed or refractory MM patients.
18
Koehler, M., R. Goorha, GR Kitchingman, GD Ayers, and J. Jr Mirro. "A monoclonal antibody to a novel surface antigen, MKW, blocks the antiproliferative and differentiation effects of granulocyte- macrophagecolony-stimulating factor and vitamin D3." Blood 80, no. 2 (July 15, 1992): 367–73. http://dx.doi.org/10.1182/blood.v80.2.367.367.
Повний текст джерелаАнотація:
Abstract A monoclonal antibody (MoAb) recognizes a novel 52-Kd cell protein (MKW) that is expressed on cells of the normal myelocytic and monocytic lineage, a subset of B cells, and the U937 cell line. Using the U937 cell line as a model, the MoAb (anti-MKW) was examined for its ability to inhibit the effects of differentiation-inducing factors. In the U937 cell line, recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) inhibits cell proliferation, 12-O- tetradecanoylphorbol-13-acetate (TPA) inhibits proliferation and induces the early differentiation antigen CD11b, and vitamin D3 inhibits proliferation and induces both CD11b and the late differentiation antigen CD14. The antiproliferative and differentiation effects of rhGM-CSF and vitamin D3 on U937 cells were inhibited by the anti-MKW MoAb. Similar effects were seen when anti-MKW antibody was added 30 minutes before or 2 hours after rhGM-CSF or vitamin D3, suggesting that its effects are not mediated by blocking or binding to the receptors for these growth factors. The anti-MKW MoAb had no effect on TPA-induced differentiation in U937 cells, indicating that TPA exerts its effects through a pathway different from rhGM-CSF and vitamin D3. These results suggest that the MKW antigen is important in controlling the proliferation and differentiation of monocytic cells.
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Akerstrom, V. L., and M. R. Walters. "Physiological effects of 1,25-dihydroxyvitamin D3 in TM4 Sertoli cell line." American Journal of Physiology-Endocrinology and Metabolism 262, no. 6 (June 1, 1992): E884—E890. http://dx.doi.org/10.1152/ajpendo.1992.262.6.e884.
Повний текст джерелаАнотація:
1,25-Dihydroxyvitamin D3 [1,25(OH)2D3] receptors have been previously described in Sertoli cells. This study was performed to assess biological activity of the receptor in the mouse Sertoli cell line TM4. A 2-h preincubation with 0.01-25 nM 1,25(OH)2D3 resulted in a dose-dependent rapid uptake of 45Ca2+ within 5 min of addition of the isotope to the cells (27 +/- 8%, n = 4 experiments; P less than 0.05). This response was specific for 1,25(OH)2D3, in that it was not induced by 25-hydroxyvitamin D3, estradiol, cortisol, R 5020 (promegestone), or testosterone. However, a combination of testosterone and 1,25(OH)2D3 inhibited uptake by 23 +/- 8% (n = 3 experiments, P less than 0.01). That the mechanism responsible for 1,25(OH)2D3-stimulated uptake may involve 1,25(OH)2D3 receptor interaction is supported by the observation that cycloheximide inhibited the response. Conversely, there was no detectable change in uptake by 1,25(OH)2D3-treated cells after 24-h incubation with 0.1-5 nM 1,25(OH)2D3. Increased levels of DNA and protein content also resulted from a 2-h incubation with the steroid and were sustained up to 24 h without a concomitant increase in cell number or a detectable change in cell morphology. The presence of specific 1,25(OH)2D3 receptor-like binding sites was demonstrated by sucrose gradient analysis and hydroxylapatite assay. These data demonstrate that 1,25(OH)2D3 may play an important role in testicular function through regulation of receptor-mediated events.
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Levavi-Sivan, Berta, Bae-Hang Park, Sara Fuchs, and C. Simone Fishburn. "Human D3 dopamine receptor in the medulloblastoma TE671 cell line: cross-talk between D1 and D3 receptors." FEBS Letters 439, no. 1-2 (November 13, 1998): 138–42. http://dx.doi.org/10.1016/s0014-5793(98)01356-8.
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Levavi-Sivan, B., C. S. Fishburn, and B. H. Park. "Human D3 dopamine receptor in the meduloblastoma TE671 cell line: Cross-talk between D1 and D3 receptors." Neuroscience Letters 237 (November 1997): S32. http://dx.doi.org/10.1016/s0304-3940(97)90132-4.
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Baudet, Christel, Guillemette Chevalier, Philippe Naveilhan, Lise Binderup, Philippe Brachet та Didier Wion. "Cytotoxic effects of 1α,25-dihydroxyvitamin D3 and synthetic vitamin D3 analogues on a glioma cell line". Cancer Letters 100, № 1-2 (лютий 1996): 3–10. http://dx.doi.org/10.1016/0304-3835(95)04054-4.
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Petty, W. J., W. R. Voelzke, V. A. Memoli, K. H. Dragnev, J. J. Urbanic, J. R. Rigas, and E. Dmitrovsky. "Expression of cyclin D3 confers resistance to erlotinib." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 18054. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.18054.
Повний текст джерелаАнотація:
18054 Background: Transcriptional repression of cyclin D1 occurs during responses to erlotinib (E) both in vitro and in vivo. Cyclin D3 has overlapping function with cyclin D1 but has distinct transcriptional regulation. Methods: The expression of cyclin D3 was compared in E sensitive cell lines (H358, H441) and an E resistant cell line (A549). Cyclins D1, D2, and D3 were independently overexpressed in E sensitive NIH 3T3 cells by plasmid transfection. Biopsy tissues from a proof-of-principal clinical trial of E were assessed for cyclin D3 expression. Results: A549 cells were resistant to E and expressed high levels of cyclin D3 RNA and protein compared to E sensitive cell lines. Overexpression of cyclin D1 and cyclin D3 conferred partial resistance to E in NIH 3T3 cells while cyclin D2 had no significant effect. Comparison of cyclin D3 immunostaining in tumor biopsies from patients before and after treatment with E revealed an increase in the percentage of cyclin D3 expressing cells following treatment with E. Conclusions: Cyclin D3 confers resistance to E in vitro and in vivo. Drugs such as retinoids and rexinoids that target cyclin D3 expression may prove useful for enhancing sensitivity to E. No significant financial relationships to disclose.
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Mustafa, Twana A., and Iman M. Rasul. "Cytotoxic Effects of Vitamin D3 on Tumor Cell Lines." Polytechnic Journal 9, no. 2 (December 1, 2019): 100–104. http://dx.doi.org/10.25156/ptj.v9n2y2019.pp100-104.
Повний текст джерелаАнотація:
Vitamin D3 is a potent antiproliferative agent against various tumor cells in vitro. Here, the results of Vitamin D3 study as a potential antitumor therapy in vitro are presented. Applying antiproliferative 3(4,5-dimethyl- 2-thiazolyl)-2,5-diphenyl-2H-terazolium bromide assays, the inhibitory effects of the Vitamin D were measured. The following cancer cell lines were employed: L20B (normal cell line) and RD (malignant rhabdomyosarcoma). Both cell lines were cultivated in 96-wells culture plates in the presence and absence of different doses of Vitamin D (10–6, 10–8, and 10–10 μg/ml) for 24 and 48 h. In vitro results of cytotoxic effects were variable on both cell lines, according to dose and exposure time, after 24 h exposure of RD, the highest concentration of Vitamin D3(10−6 μg/ml) treatment had significant effect in decreasing cell proliferation from O.D (0.4570 ± 0.0302) to (0.1540 ± 0.0017) as compared with negative control, with increasing concentrations the cytotoxicity is increased directly proportional; thus, the lowest cytotoxic effect was at the lowest concentration of both Vitamin D3 (10−12 μg/ml). While after 48 h, the same concentration of Vitamin D3 shows an increase in proliferation from 0.3710 ± 0.0023 to 0.4597 ± 0.0017 on the RD cell line. While a significant increase in L20B cell proliferation was observed after 24 h treatment at the concentration (10−6 μg/ml) from 0.3570 ± 0.0011 to 0.0330 ± 0.0017, when compared with the negative control. However, after 48 h treatment, a significant increases the proliferation of cells as shown from O.D 0.2927 ± 0.0008 to 0.4300 ± 0.0011, respectively. Thus, the present study was aimed to evaluate the antiproliferative property of Vitamin D and its relation to inhibition of cancer cell growth.
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Rockett, Kirk A., Roger Brookes, Irina Udalova, Vincent Vidal, Adrian V. S. Hill, and Dominic Kwiatkowski. "1,25-Dihydroxyvitamin D3 Induces Nitric Oxide Synthase and Suppresses Growth of Mycobacterium tuberculosis in a Human Macrophage-Like Cell Line." Infection and Immunity 66, no. 11 (November 1, 1998): 5314–21. http://dx.doi.org/10.1128/iai.66.11.5314-5321.1998.
Повний текст джерелаАнотація:
ABSTRACT Inducible synthesis of nitric oxide (NO) by macrophages is an important mechanism of the host defense against intracellular infection in mice, but the evidence for significant levels of inducible NO production by human macrophages is controversial. Here we report that the human promyelocytic cell line HL-60, when differentiated to a macrophage-like phenotype, acquires the ability to produce substantial amounts of NO on stimulation with LPS or 1,25-dihydroxyvitamin D3 (1,25-D3) in the absence of activating factors such as gamma interferon. Expression of the inducible nitric oxide synthase (NOS2) was confirmed by sequencing of the reverse transcription-PCR product from stimulated HL-60 cells. Kinetic studies after lipopolysaccharide stimulation show that NOS2 mRNA levels rise within 3 to 6 h, that conversion of [14C]arginine to [14C]citrulline is maximal at 5 to 6 days, and that levels of reactive nitrogen intermediates stabilize at around 20 μM at 7 to 8 days. We find that 1,25-D3 acts to suppress the growth of Mycobacterium tuberculosis in these cells and that this effect is inhibited byN G-monomethyl-l-arginine, suggesting that vitamin D-induced NO production may play a role in the host defense against human tuberculosis.
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Ott, M. Michaela, Jirina Bartkova, Jiri Bartek, Alexander Dürr, Lars Fischer, German Ott, Hans Konrad Müller-Hermelink, and Hans Kreipe. "Cyclin D1 Expression in Mantle Cell Lymphoma Is Accompanied by Downregulation of Cyclin D3 and Is Not Related to the Proliferative Activity." Blood 90, no. 8 (October 15, 1997): 3154–59. http://dx.doi.org/10.1182/blood.v90.8.3154.
Повний текст джерелаАнотація:
Abstract The cell cycle regulatory protein cyclin D1 is essential for G1-S phase transition in several epithelial and mesenchymal tissues but is apparently not essential in normal mature B cells. An overexpression of cyclin D1 is induced by the chromosomal translocation t(11; 14)(q13; q32), which characterizes non-Hodgkin's lymphomas (NHLs) of mantle cell type. We studied 26 cases of mantle cell lymphoma (MCL) for the expression of cyclins D1 and D3. A total of 23 lymphomas showed a nuclear staining for cyclin D1, whereas reactive B cells of residual germinal centers were constantly negative. When compared with cyclin D3, an inverse staining pattern emerged. Whereas the B cells of residual germinal centers reacted strongly positive for cyclin D3, there was low or missing expression of cyclin D3 in MCL cells. In other B-cell lymphomas (n = 55), including chronic lymphocytic leukemia, low-grade lymphomas of mucosa-associated lymphatic tissue, follicular lymphomas, and diffuse large B-cell lymphomas, no cyclin D1 expression could be detected and 89% of these cases displayed cyclin D3 positivity. Lymphoma cell lines harboring the t(11; 14) showed cyclin D1 protein but no or very low levels of cyclin D3; three other B-cell lines, a T-cell line, and peripheral blood lymphocytes strongly expressed cyclin D3 and reacted negatively for cyclin D1. We conclude that the chromosomal translocation t(11; 14) leads to an abnormal protein expression of cyclin D1 in the tumor cells of MCL and induces a consecutive downregulation of cyclin D3. In contrast to other B-NHLs, cyclin D1 and D3 expression in MCL is not related to the growth fraction.
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Miller, Barbara E., David P. Chin, and Glenville Jones. "1,25-dihydroxyvitamin D3 metabolism in a human osteosarcoma cell line and human bone cells." Journal of Bone and Mineral Research 5, no. 6 (December 3, 2009): 597–608. http://dx.doi.org/10.1002/jbmr.5650050609.
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Zhao, Fang, Antonina Vilardi, Robert J. Neely, and John Kim Choi. "Promotion of Cell Cycle Progression by Basic Helix-Loop-Helix E2A." Molecular and Cellular Biology 21, no. 18 (September 15, 2001): 6346–57. http://dx.doi.org/10.1128/mcb.21.18.6346-6357.2001.
Повний текст джерелаАнотація:
ABSTRACT Normal B-cell development requires the E2A gene and its encoded transcription factors E12 and E47. Current models predict that E2A promotes cell differentiation and inhibits G1 cell cycle progression. The latter raises the conundrum of how B cells proliferate while expressing high levels of E2A protein. To study the relationship between E2A and cell proliferation, we established a tissue culture-based model in which the activity of E2A can be modulated in an inducible manner using E47R, an E47-estrogen fusion construct, and E47ERT, a dominant negative E47-estrogen fusion construct. The two constructs were subcloned into retroviral vectors and expressed in the human pre-B-cell line 697, the human myeloid progenitor cell line K562, and the murine fibroblastic cell line NIH 3T3. In both B cells and non-B cells, suppression of E2A activity by E47ERT inhibited G1 progression and was associated with decreased expression of multiple cyclins including the G1-phase cyclin D2 and cyclin D3. Consistent with these findings, E2A null mice expressed decreased levels of cyclin D2 and cyclin D3 transcripts. In complementary experiments, ectopic expression of E47R promoted G1 progression and was associated with increased levels of multiple cyclins, including cyclin D2 and cyclin D3. The induction of some cyclin transcripts occurred even in the absence of protein synthesis. We conclude that, in some cells, E2A can promote cell cycle progression, contrary to the present view that E2A inhibits G1 progression.
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Mason, Shelley S., Sean S. Kohles, Shelley R. Winn, and Randy D. Zelick. "Extrahepatic 25-Hydroxylation of Vitamin D3 in an Engineered Osteoblast Precursor Cell Line Exploring the Influence on Cellular Proliferation and Matrix Maturation during Bone Development." ISRN Biomedical Engineering 2013 (June 4, 2013): 1–11. http://dx.doi.org/10.1155/2013/956362.
Повний текст джерелаАнотація:
Osteoblastic precursors experience distinct stages during differentiation and bone development, which include proliferation, extracellular matrix (ECM) maturation, and ECM mineralization. It is well known that vitamin D plays a large role in the regulation of bone mineralization and homeostasis via the endocrine system. The activation of vitamin D requires two sequential hydroxylation steps, first in the kidney and then in the liver, in order to carry out its role in calcium homeostasis. Recent research has demonstrated that human-derived mesenchymal stem cells (MSCs) and osteoblasts can metabolize the immediate vitamin D precursor 25-dihydroxyvitamin D3 (25OHD3) to the active steroid 1α,25-dihydroxyvitamin D3 (1,25OH2D3) and elicit an osteogenic response. However, reports of extrahepatic metabolism of vitamin D3, the parental vitamin D precursor, have been limited. In this study, we investigated whether osteoblast precursors have the capacity to convert vitamin D3 to 1,25OH2D3 and examined the potential of vitamin D3 to induce 1,25OH2D3 associated biological activities in osteoblast precursors. It was demonstrated that the engineered osteoblast precursor derived from human marrow (OPC1) is capable of metabolizing vitamin D3 to 1,25OH2D3 in a dose-dependent manner. It was also demonstrated that administration of vitamin D3 leads to the increase in alkaline phosphatase (ALP) activity associated with osteoblast ECM maturation and calcium deposits and a decrease in cellular proliferation in both osteoblast precursor cell lines OPC1 and MC3T3-E1. These findings provide a two-dimensional culture foundation for future three-dimensional engineered tissue studies using the OPC1 cell line.
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Teramachi, Jumpei, Noriyoshi Kurihara, John M. Chirgwin, and G. David Roodman. "The Increased 1,25-(OH)2D3 Sensitivity of Myeloma Cells and Marrow Stromal Cells Enhances RANKL Production and Tumor Cell Growth." Blood 120, no. 21 (November 16, 2012): 3946. http://dx.doi.org/10.1182/blood.v120.21.3946.3946.
Повний текст джерелаАнотація:
Abstract Abstract 3946 Vitamin D plays multiple roles in normal and malignant cell function, regulating cell differentiation and proliferation as well as bone homeostasis. Epidemiologic studies suggest that low levels of vitamin D contribute to the progression of lung cancer, breast cancer, colorectal and prostate cancer as well as lymphoma and melanoma. However, the role of vitamin D in multiple myeloma (MM) is unclear. In contrast to its growth inhibition of solid tumors, vitamin D has little anti-proliferative effects on MM cells. The physiological responses of myeloma cells to vitamin D are unknown, as are its effects on the marrow microenvironment in myeloma bone disease. Vitamin D insufficiency or deficiency has been documented in the majority of myeloma patients. Vitamin D receptor (VDR) is expressed by RPMI8226 cells, but it is unknown if this is a common finding in MM. Further, the functional consequences of VDR expression in myeloma cells are not well characterized. We reported osteoclast (OCL) precursors from patients with Paget's disease (PD) of bone were hypersensitive to 1,25-(OH)2D3 (1,25-D3) and formed OCL at physiologic concentrations of 1,25-D3 rather than the pharmacologic concentrations of 1,25-D3 required for normal OCL formation in vitro. This enhanced sensitivity to 1,25-D3 was due to increased expression of a novel VDR co-activator, TAF12, a member of the TFIID transcription complex. We found TAF12 expression was increased in marrow stromal cells (BMSC) by increased NFκB signaling and enhanced the capacity of BMSC to produce RANKL in response to low levels of 1,25-D3. Because the marrow microenvironment in MM and PD has many similarities in terms of increased OCL activity and enhanced NFκB signaling, we determined if MM cells induced TAF12 expression in BMSC of MM patients and if 1,25-D3 could enhanced RANKL production in BMSC of MM patients, even in patients with low levels of 1,25-D3. We found that both BMSC and CD138+ primary myeloma cells from MM patients expressed increased TAF12 levels compared to normal BMSC and CD138+ bone marrow cells. Four of four human MM cell lines (MM1.S, ANBL6, JJN3 and RPMI8266) expressed VDR, TAF12 and ATF7, which potentiates TAF12-mediated gene transcription. MM1.S and JJN3 but not RPMI8266 produced increased amounts of RANKL in response to very low levels of 1,25-D3. Further, 1,25-D3 increased VEGF, DKK1 and α4β1 integrin expression by MM1.S, JJN3 and RPMI8266 cells and enhanced adhesive interactions between MM cells and BMSC that increase MM growth. To confirm the role of TAF12 in the increased RANKL expression by MM cells treated with 1,25-D3, we established a stable TAF12 anti-sense JJN3 cell line (AS-TAF12-JJN3). AS-TAF12-JJN3 cells had markedly decreased RANKL production, VDR content and CYP24A1 accumulation in response to 1,25-D3. MM1.S and JJN3 myeloma cells treated with a VDR antagonist (TEI-9647) decreased RANKL production and α4β1 integrin expression in response to low levels of 1,25-D3. Further, 1,25-D3 induced VCAM-1 expression on normal human BMSC. Co-culture of JJN3 cells with BMSC treated with 1,25-D3 induced both MM cell growth and cell adhesion. In contrast, co-culture with AS-TAF12-JJN3 cells resulted in decreased cell growth and cell adhesion. Further, 1,25-D3 treatment of mouse OCL precursors co-cultured with JJN3 cells, but not AS-TAF12-JJN3 cells, increased OCL formation. These results suggest that increased TAF12 levels in MM cells and BMSC allow low levels of 1,25-D3 significantly to increase RANKL production by both MM cells and BMSC, and enhance adhesive interactions between MM cells and BMSC, thus increasing MM cell growth and OCL formation. Disclosures: No relevant conflicts of interest to declare.
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Naveilhan, Philippe, Isabelle Neveu, Didier Wion, and Philippe Brachet. "1,25-Dihydroxyvitamin D3, an inducer of glial cell line-derived neurotrophic factor." NeuroReport 7, no. 13 (September 1996): 2171–75. http://dx.doi.org/10.1097/00001756-199609020-00023.
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Stenson, William F., Steven L. Teitelbaum, and Zvi Bar-Shavit. "Arachidonic acid metabolism by a vitamin D3-differentiated human leukemic cell line." Journal of Bone and Mineral Research 3, no. 5 (December 3, 2009): 561–71. http://dx.doi.org/10.1002/jbmr.5650030513.
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Fasler-Kan, Elizaveta, Claudia Suenderhauf, Natasha Barteneva, Birk Poller, Daniel Gygax, and Jörg Huwyler. "Cytokine signaling in the human brain capillary endothelial cell line hCMEC/D3." Brain Research 1354 (October 2010): 15–22. http://dx.doi.org/10.1016/j.brainres.2010.07.077.
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Zhang, Wenqing, Daniele Bergamaschi, Boquan Jin, and Xin Lu. "Posttranslational modifications of p27kip1 determine its binding specificity to different cyclins and cyclin-dependent kinases in vivo." Blood 105, no. 9 (May 1, 2005): 3691–98. http://dx.doi.org/10.1182/blood-2003-07-2558.
Повний текст джерелаАнотація:
AbstractUsing 2-dimensional gel electrophoresis (2D-gel) analysis, we show here that cell-cycle entry is associated with a significant increase in p27kip1 phosphorylation in human primary B cells. A similar pattern of increase in p27kip1 phosphorylation was also seen in 2 fast-growing tumor cell lines, Burkitt lymphoma cell line BL40 and breast carcinoma cell line Cal51, where inactive p27kip1 is expressed at high levels. Detailed analysis revealed for the first time that different cyclins and cyclin-dependent kinases (cdk's) interact with distinct posttranslationally modified isoforms of p27kip1 in vivo. Cyclin E but not cyclin A selectively interacts with phosphorylated p27kip1 isoforms, while cyclin D1 and D2 favor unphosphorylated p27kip1 isoforms in vivo. Interestingly, cyclin D3 and cdk4 selectively interact with phosphorylated p27kip1 in BL40 cells. Among all D-type cyclin/cdk4 and cdk6 complexes, cyclin D3/cdk4 is most active in sequestering the inhibitory activity of p27kip1 in vitro in a cyclinE/cdk2 kinase assay. This novel feature of the binding specificity of p27kip1 to cyclins and cdk's in vivo is interpreted in the context of overexpression of cyclin D3 in the presence of high levels of p27kip1 in human B-cell lymphomas with adverse clinical outcome.
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Cortes, Mauricio, Kelsey Natsuhara, Wolfram Goessling, and Trista E. North. "Vitamin D3 Modulates Definitive Hematopoiesis by Two Distinct Mechanisms in the Developing Zebrafish Embryo." Blood 120, no. 21 (November 16, 2012): 763. http://dx.doi.org/10.1182/blood.v120.21.763.763.
Повний текст джерелаАнотація:
Abstract Abstract 763 Studies of the vitamin D3 signaling pathway have revealed a broad role for this hormone in tissue homeostasis and as a result there is great interest in exploring the therapeutic potential of vitamin D3 for the treatment of various diseases including cancer. Studies investigating the role of vitamin D3 in hematological malignancies have shown that in vitro vitamin D3 has anti-proliferative and pro-differentiation effects resulting in differentiation of leukemic cell lines towards the monocytic lineage. Surprisingly, the role of vitamin D3 in HSC homeostasis and leukemia progression in vivo is not well understood. To elucidate the mechanisms of action of vitamin D3 in vivo during HSC self-renewal and differentiation, we utilized the zebrafish (Danio rerio) as vertebrate model due to their evolutionary conserved blood system and their amenability for genetic and chemical manipulation. Vitamin D3 was identified in a chemical screen performed in our laboratory as a regulator of runx1 and c-myb expression in the aorta-gonad mesonephros (AGM), the first site of definitive hematopoiesis. Treatments of zebrafish embryos with active vitamin D3 (1,25OH D3) between 12–36 hours post fertilization (hpf) resulted in increased expression of HSC markers (runx1, c-myb, CD41) as determined by whole mount in situ hybridization (WISH). In contrast, treatment with the non-hydroxylated vitamin D3 precursor cholecalciferol (D3) resulted in decreased runx1 and c-myb expression. D3 treatment during HSC induction and expansion from 24–36 hpf did not affect runx1 and c-myb expression, suggesting that D3 is acting early during the establishment of the vascular niche. To quantify the difference in HSC progenitors observed by WISH, FACS analysis was performed on double positive Tg(Lmo2:dsRed), Tg(c-myb:gfp) embryos. 1,25OH D3 treated embryos had a 20% increase in the double positive cell population corresponding to HSCs, while treatment with D3 resulted in a 25% decrease in the number of HSCs. The differential effect of 1,25OH D3 and D3 suggest that these two compounds act via two distinct mechanisms. To determine if the HSC enhancement observed by 1,25OH D3 was acting through the canonical vitamin D3 receptor (VDR), loss of function experiments were performed by injecting morpholinos targeting the vitamin D receptors. Morpholino knockdown of VDRA and VDRB (zebrafish VDR orthologs) resulted in decreased expression of runx1 c-myb, and CD41 via WISH. The decrease in HSC positive cells was confirmed by fluorescence microscopy using the Tg(Runx1P2:gfp) and Tg(-6.0itga:gfp) reporter lines, further supporting our hypothesis. To address the decrease in HSCs by D3, we postulated that D3 was inhibiting hedgehog signaling, as vitamin D3 has been previously shown to act as a negative regulator of the hedgehog pathway. In support of our hypothesis, treatment with D3 resulted in decreased ptch2 mRNA expression a downstream target of hedgehog signaling. In addition, FACS analysis using the hedgehog reporter Tg(6xGli:mCherry) line showed a 15% reduction in the number of mCherry positive cells in D3 treated embryos compared to controls. Co-treatments of zebrafish embryos with the hedgehog antagonist cyclopamine and D3 resulted in additive loss of reporter activity (45%) and loss of runx1 positive cells in the AGM, revealing synergy between these two compounds. In addition, co-exposure with the hedgehog agonist SAG rescued the HSC defect in D3-treated embryos. Hedgehog signaling is known to regulate vein and artery specification through the activation of notch signaling. Consistent with our hypothesis that D3 reduces hedgehog signaling, an expansion of the venous marker flt4 and a reduction in the expression of the arterial marker ephrinb2a was observed by WISH on D3-treated embryos. Furthermore, treatment of the notch reporter line Tg(Notch:gfp) with D3 resulted in lowered notch activity. In summary, these studies reveal that the active 1,25OH D3 positively regulates HSC progenitors in vivo during the onset of definitive hematopoiesis. In contrast, the non-hydroxylated vitamin D3 precursor acts as negative regulator of hematopoiesis by inhibiting hedgehog signaling and affecting vascular niche formation. Based on our studies, the differential effect between D3 and 1,25OH D3 should be considered when investigating the therapeutic potential of vitamin D3 in the context of hematological malignancies and other cancers. Disclosures: Goessling: Fate Therapeutics: Consultancy. North:Fate Therapeutics: Consultancy.
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Mawer, E. B. "Constitutive synthesis of 1,25-dihydroxyvitamin D3 by a human small cell lung cancer cell line." Journal of Clinical Endocrinology & Metabolism 79, no. 2 (August 1, 1994): 554–60. http://dx.doi.org/10.1210/jc.79.2.554.
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Mawer, E. B., M. E. Hayes, S. E. Heys, M. Davies, A. White, M. F. Stewart, and G. N. Smith. "Constitutive synthesis of 1,25-dihydroxyvitamin D3 by a human small cell lung cancer cell line." Journal of Clinical Endocrinology & Metabolism 79, no. 2 (August 1994): 554–60. http://dx.doi.org/10.1210/jcem.79.2.8045976.
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Green, J., K. V. Luong, C. R. Kleeman, L. H. Ye, and C. Chaimovitz. "1,25-Dihydroxyvitamin D3 inhibits Na(+)-dependent phosphate transport in osteoblastic cells." American Journal of Physiology-Cell Physiology 264, no. 2 (February 1, 1993): C287—C295. http://dx.doi.org/10.1152/ajpcell.1993.264.2.c287.
Повний текст джерелаАнотація:
In the present work we investigated the influence of vitamin D3 metabolites on Na(+)-dependent phosphate (Pi) transport in the clonal osteoblastic cell line UMR-106. The vitamin D3 metabolite 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] dose-dependently inhibited Pi transport with a half-maximal concentration of approximately 5 x 10(-11) M. The effect of 1,25(OH)2D3 was first observed after 8 h of preincubation period. Inhibition of phosphate uptake was relatively specific for the 1,25(OH)2D3 analogue of vitamin D3. The potency order was 1,25(OH)2D3 >> 24,25-dihydroxyvitamin D3 > 25-[3H]hydroxyvitamin D3. Kinetically, 1,25(OH)2D3 decreased the maximal velocity of the phosphate uptake system, whereas the affinity for phosphate was unaffected. Activation of protein kinase C (PKC) in UMR-106 cells stimulated Na(+)-dependent Pi transport. Nonetheless, the inhibitory effect of 1,25(OH)2D3 on Pi transport was not related to downregulation of PKC. Chemical determination of intracellular Pi showed a 50% reduction after 24-h preincubation with 10(-8) M 1,25(OH)2D3. We conclude that 1,25(OH)2D3 inhibits Na(+)-dependent phosphate transport in osteoblastic cells. This in turn leads to intracellular Pi depletion. The physiological implication of this phenomenon on the effects of vitamin D on osteoblasts in situ is discussed.
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Jensen, Simon Skjøde, Mogens Winkel Madsen, Jiri Lukas, Lise Binderup та Jiri Bartek. "Inhibitory Effects of 1α,25-Dihydroxyvitamin D3 on the G1–S Phase-Controlling Machinery". Molecular Endocrinology 15, № 8 (1 серпня 2001): 1370–80. http://dx.doi.org/10.1210/mend.15.8.0673.
Повний текст джерелаАнотація:
Abstract The nuclear hormone 1α,25-dihydroxyvitamin D3 induces cell cycle arrest, differentiation, or apoptosis depending on target cell type and state. Although the antiproliferative effect of 1α,25-dihydroxyvitamin D3 has been known for years, the molecular basis of the cell cycle blockade by 1α,25-dihydroxyvitamin D3 remains largely unknown. Here we have investigated the mechanisms underlying the G1 arrest induced upon 1α,25-dihydroxyvitamin D3 treatment of the human breast cancer cell line MCF-7. Twenty-four-hour exposure of exponentially growing MCF-7 cells to 1α,25-dihydroxyvitamin D3 impeded proliferation by preventing S phase entry, an effect that correlated with appearance of the growth-suppressing, hypophosphorylated form of the retinoblastoma protein (pRb), and modulation of cyclin-dependent kinase (cdk) activities of cdk-4, -6, and -2. Time course immunochemical and biochemical analyses of the cellular and molecular effects of 1α,25-dihydroxyvitamin D3 treatment for up to 6 d revealed a dynamic chain of events, preventing activation of cyclin D1/cdk4, and loss of cyclin D3, which collectively lead to repression of the E2F transcription factors and thus negatively affected cyclin A protein expression. While the observed 10-fold inhibition of cyclin D1/cdk 4-associated kinase activity appeared independent of cdk inhibitors, the activity of cdk 2 decreased about 20-fold, reflecting joint effects of the lower abundance of its cyclin partners and a significant increase of the cdk inhibitor p21CIP1/WAF1, which blocked the remaining cyclin A(E)/cdk 2 complexes. Together with a rapid down-modulation of the c-Myc oncoprotein in response to 1α,25-dihydroxyvitamin D3, these results demonstrate that 1α,25-dihydroxyvitamin D3 inhibits cell proliferation by targeting several key regulators governing the G1/S transition.
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Piatek, Karina, Andrzej Kutner, Dan Cacsire Castillo-Tong, Teresa Manhardt, Nadja Kupper, Urszula Nowak, Michał Chodyński, Ewa Marcinkowska, Enikö Kallay, and Martin Schepelmann. "Vitamin D Analogs Regulate the Vitamin D System and Cell Viability in Ovarian Cancer Cells." International Journal of Molecular Sciences 23, no. 1 (December 24, 2021): 172. http://dx.doi.org/10.3390/ijms23010172.
Повний текст джерелаАнотація:
Background: Ovarian cancer (OC) is one of the most lethal cancers in women. The active form of vitamin D3, 1,25-dihydroxyvitamin D3 (1,25D3, calcitriol) has anticancer activity in several cancers, including ovarian cancer, but the required pharmacological doses may cause hypercalcemia. We hypothesized that newly developed, low calcemic, vitamin D analogs (an1,25Ds) may be used as anticancer agents instead of calcitriol in ovarian cancer cells. Methods: We used two patient-derived high-grade serous ovarian cancer (HGSOC) cell lines with low (13781) and high (14433) mRNA expression levels of the gene encoding 1,25-dihydroxyvitamin D3 24-hydroxylase CYP24A1, one of the main target genes of calcitriol. We tested the effect of calcitriol and four structurally related series of an1,25Ds (PRI-1906, PRI-1907, PRI-5201, PRI-5202) on cell number, viability, the expression of CYP24A1, and the vitamin D receptor (VDR). Results: CYP24A1 mRNA expression increased in a concentration-dependent manner after treatment with all compounds. In both cell lines, after 4 h, PRI-5202 was the most potent analog (in 13781 cells: EC50 = 2.98 ± 1.10 nmol/L, in 14433 cells: EC50 = 0.92 ± 0.20 nmol/L), while PRI-1907 was the least active one (in 13781 cells: EC50 = n/d, in 14433 cells: EC50 = n/d). This difference among the analogs disappeared after 5 days of treatment. The 13781 cells were more sensitive to the an1,25Ds compared with 14433 cells. The an1,25Ds increased nuclear VDR levels and reduced cell viability, but only in the 13781 cell line. Conclusions: The an1,25Ds had different potencies in the HGSOC cell lines and their efficacy in increasing CYP24A1 expression was cell line- and chemical structure-dependent. Therefore, choosing sensitive cancer cell lines and further optimization of the analogs’ structure might lead to new treatment options against ovarian cancer.
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Elstner, E., YY Lee, M. Hashiya, S. Pakkala, L. Binderup, AW Norman, WH Okamura, and HP Koeffler. "1 alpha,25-Dihydroxy-20-epi-vitamin D3: an extraordinarily potent inhibitor of leukemic cell growth in vitro." Blood 84, no. 6 (September 15, 1994): 1960–67. http://dx.doi.org/10.1182/blood.v84.6.1960.1960.
Повний текст джерелаАнотація:
Abstract We have evaluated seven recently synthesized vitamin D3 analogs for their abilities to inhibit clonal growth of leukemic cells, to induce leukemic cell differentiation, to stimulate clonal growth of normal myeloid committed stem cells, and to transactivate a reporter gene having a 1,25(OH)2D3 response element (VDRE). The 1,25(OH)2–20-epi-D3 showed extraordinary activity; at 10(-11) mol/L it inhibited clonal growth of 87% of HL-60 myeloblast cells, 60% of S-LB1 cells (human T- cell lymphotropic virus type 1 [HTLV-1]-immortalized human T-lymphocyte cell line) and 50% of leukemic clonogenic cells (colony-forming unit- leukemia) obtained from patients with acute myelogenous leukemia. No effect of either 1,25(OH)2D3 or 1,25(OH)2–20-epi-D3 was observed on the clonal proliferation of an HTLV-1-immortalized human T-lymphocyte cell line (Ab-VDR) having nonfunctional 1,25 (OH)2D3 cellular receptors (VDR). The abilities of 1,25(OH)2–20-epi-D3 to induce differentiation of HL-60 cells, as measured by generation of superoxide and nonspecific esterase production, was less than its antiproliferative activities. This analog stimulated colony-forming unit-granulocyte-macrophage growth from normal human bone marrow. To gain insights into the remarkable antileukemic activities of 1,25(OH)2–20-epi-D3, we examined its ability to enter HL-60 cells, bind to the VDR, and interact with a transfected VDRE attached upstream of a TK promoter-driven reporter gene (chloramphenicol acetyl transferase [CAT]). The 1,25(OH)2–20-epi- D3 potently increased CAT activity (> 16-fold, as compared with cells transfected with control receptor having no VDRE); paradoxically, 1,25(OH)2–20-epi-D3 was of equal potency to 1,25(OH)2D3 in transactivating the VDRE-containing reporter gene, even though the analog had a 1,000-fold greater antileukemic effect as compared with 1,25(OH)2D3. In summary, we have identified an extremely potent 1,25(OH)2D3 analog with antiproliferative and differentiating effects on leukemic cells and that may be clinically useful. This analog appears to generate biologic responses via the classical VDR pathway, but further studies are required to elucidate the mechanism by which this analog produces its prominent activities.
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Elstner, E., YY Lee, M. Hashiya, S. Pakkala, L. Binderup, AW Norman, WH Okamura, and HP Koeffler. "1 alpha,25-Dihydroxy-20-epi-vitamin D3: an extraordinarily potent inhibitor of leukemic cell growth in vitro." Blood 84, no. 6 (September 15, 1994): 1960–67. http://dx.doi.org/10.1182/blood.v84.6.1960.bloodjournal8461960.
Повний текст джерелаАнотація:
We have evaluated seven recently synthesized vitamin D3 analogs for their abilities to inhibit clonal growth of leukemic cells, to induce leukemic cell differentiation, to stimulate clonal growth of normal myeloid committed stem cells, and to transactivate a reporter gene having a 1,25(OH)2D3 response element (VDRE). The 1,25(OH)2–20-epi-D3 showed extraordinary activity; at 10(-11) mol/L it inhibited clonal growth of 87% of HL-60 myeloblast cells, 60% of S-LB1 cells (human T- cell lymphotropic virus type 1 [HTLV-1]-immortalized human T-lymphocyte cell line) and 50% of leukemic clonogenic cells (colony-forming unit- leukemia) obtained from patients with acute myelogenous leukemia. No effect of either 1,25(OH)2D3 or 1,25(OH)2–20-epi-D3 was observed on the clonal proliferation of an HTLV-1-immortalized human T-lymphocyte cell line (Ab-VDR) having nonfunctional 1,25 (OH)2D3 cellular receptors (VDR). The abilities of 1,25(OH)2–20-epi-D3 to induce differentiation of HL-60 cells, as measured by generation of superoxide and nonspecific esterase production, was less than its antiproliferative activities. This analog stimulated colony-forming unit-granulocyte-macrophage growth from normal human bone marrow. To gain insights into the remarkable antileukemic activities of 1,25(OH)2–20-epi-D3, we examined its ability to enter HL-60 cells, bind to the VDR, and interact with a transfected VDRE attached upstream of a TK promoter-driven reporter gene (chloramphenicol acetyl transferase [CAT]). The 1,25(OH)2–20-epi- D3 potently increased CAT activity (> 16-fold, as compared with cells transfected with control receptor having no VDRE); paradoxically, 1,25(OH)2–20-epi-D3 was of equal potency to 1,25(OH)2D3 in transactivating the VDRE-containing reporter gene, even though the analog had a 1,000-fold greater antileukemic effect as compared with 1,25(OH)2D3. In summary, we have identified an extremely potent 1,25(OH)2D3 analog with antiproliferative and differentiating effects on leukemic cells and that may be clinically useful. This analog appears to generate biologic responses via the classical VDR pathway, but further studies are required to elucidate the mechanism by which this analog produces its prominent activities.
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Hodgins, M. B., and S. Murad. "1,25-DIHYDROXYCHOLECALCIFEROL STIMULATES CONVERSION OF ANDROSTENEDIONE INTO OESTRONE BY HUMAN SKIN FIBROBLASTS IN CULTURE." Journal of Endocrinology 110, no. 1 (July 1986): R1—R4. http://dx.doi.org/10.1677/joe.0.110r001.
Повний текст джерелаАнотація:
ABSTRACT Pre-incubation of monolayer cultures of human skin fibroblasts with 1,25-dihydroxycholecalciferol (1,25-D3; 0.1-10 nmol/l) increased the rate of conversion of androstenedione into oestrone (aromatase activity) when measured subsequently in the presence of a 5α-reductase inhibitor (10 umol/l). Maximal stimulation (14- to 89-fold with 10 nmol 1,25-D3/l) occurred 12 h after addition of the hormone and was maintained for up to 48 h. Stimulation was prevented by cycloheximide. In one cell line high 1,25-D3 concentrations (>30 nmol/l)prevented the increase in aromatase activity; this did not appear to result from direct enzyme inhibition by 1,25-D3. The possibility is considered that 1,25-D3 could act as a physiological regulator of peripheral aromatase. As oestrogens can prevent postmenopausal bone loss, it is speculated that 1,25-D3 might protect against bone resorption by maintaining peripheral oestrogen biosynthesis.
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Aziz, Muhammad Alamsyah, Sofie Rifayani Krisnadi, Budi Setiabudiawan, and Budi Handono. "Effect of Vitamin D3 Treatment on Genes Expression of Corticotrophin Releasing Hormone (CRH), CRH Receptor 1 (CRH-R1) and Connexin-43 (CON-43) in PHM1-41 Cell Line that Induced by Hypoxia." Trends in Sciences 19, no. 20 (October 11, 2022): 6236. http://dx.doi.org/10.48048/tis.2022.6236.
Повний текст джерелаАнотація:
Introduction: Hypothalamic-Pituitary-Adrenal (HPA) axis activity is one of pathophysiologic mechanism that caused preterm labor. Biologic maternal stress, for instance hypoxia condition, is one of the causes that can trigger preterm birth occasion through the activation of HPA axis. It increases Corticotrophin Releasing Hormone (CRH), CRH receptor 1 (CRH-R1), and Connexin-43 (CON-43) as the trigger of the contraction process. Vitamin D as a source of Ca2+ ion is needed for myometrium smooth muscle’s concentrations and relaxation mechanism. The aim of this study was to determine the effect of vitamin D3 in PHM1-41 cell line. Materials and Methods: The human smooth muscle uterine myometrium cell line PHM1-41 as an in vitro model experimental subject, treated by hypoxia oxidative stress condition and added by vitamin D3 (5, 10, 50 and 150 nM). The dichlorodihydrofluorescein diacetate (DCFDA) fluorescent was used to measure the level of intracellular reactive oxygen species (ROS). In addition, RNA of treated PHM1-41cells was isolated for analyzing gene expressions such as CRH, CRH-R1, and CON-43 as a profile of contractility regulation. Results: ROS level effectively decrease in the cells that treated by 150 nM vitamin D3 group compared to the control hypoxia cell group (7.16 ± 0.23 and 19.49 ± 1.76, respectively). Expression of CRH, CRH-R1, and CON-43 genes are also decrease by treated with 150 nM vitamin D3 to the cells. Pearson (parametric) correlation analysis evidenced a negative correlation between the vitamin D3 additional treated to the lower of ROS level, CRH, CRH-R1, and CON-43 genes expression on PHM1-41 cell line that induced by oxidative stress condition. Conclusion: The concentration of 150 nM vitamin D3 was a prominent potency to prevent the incidence of preterm labor.
HIGHLIGHTS
Hypothalamic-Pituitary-Adrenal (HPA) axis is one of the causes of preterm birth that marked by high level of intracellular ROS leads to increasing of Corticotrophin Releasing Hormone (CRH) which has significant role in aterm and preterm labor
PHMI-41 cells can describe the Corticotrophin Releasing Hormone (CRH), CRH receptor 1 (CRH-R1), and Connexin-43 (CON-43) genes expression level so it was used as model of human pregnancy condition
Vitamin D3 is one of antioxidant agent that can decrease ROS level also CRH, CRH-R1, and CON-43 genes expression on PHM1-41 cell especially at doses of 150 nM which shown a prominent potency to prevent the preterm labor incidence
GRAPHICAL ABSTRACT
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Laemmle, Lillian L., Justus B. Cohen, and Joseph C. Glorioso. "Constitutive Expression of GATA4 Dramatically Increases the Cardiogenic Potential of D3 Mouse Embryonic Stem Cells." Open Biotechnology Journal 10, no. 1 (June 30, 2016): 248–57. http://dx.doi.org/10.2174/1874070701610010248.
Повний текст джерелаАнотація:
The transcription factor GATA binding protein 4 (GATA4) is a vital regulator of cardiac programming that acts by inducing the expression of many different genes involved in cardiomyogenesis. Here we generated a D3 mouse embryonic stem cell line that constitutively expresses high levels of GATA4 and show that these cells have dramatically increased cardiogenic potential compared to an eGFP-expressing control cell line. Embryoid bodies (EB) derived from the D3-GATA4 line displayed increased levels of cardiac gene expression and showed more abundant cardiomyocyte differentiation than control eGFP EB. These cells and two additional lines expressing lower levels of GATA4 provide a platform to screen previously untested cardiac genes and gene combinations for their ability to further increase the efficiency of cardiomyocyte differentiation beyond that achieved by transgenic GATA4 alone. Non-integrative delivery of identified gene combinations will aid in the production of differentiated cells for the treatment of ischemic cardiomyopathy.
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Makin, G., D. Lohnes, V. Byford, R. Ray, and G. Jones. "Target cell metabolism of 1,25-dihydroxyvitamin D3 to calcitroic acid. Evidence for a pathway in kidney and bone involving 24-oxidation." Biochemical Journal 262, no. 1 (August 15, 1989): 173–80. http://dx.doi.org/10.1042/bj2620173.
Повний текст джерелаАнотація:
1,25-dihydroxyvitamin D3 is converted to calcitroic acid before being excreted in the bile. Biosynthesis of calcitroic acid has been demonstrated in two target cells of vitamin D, in the kidney and the osteoblastic cell line UMR-106. Calcitroic acid was identified by combinations of h.p.l.c., u.v. spectroscopy and mass spectrometry. Evidence is presented that calcitroate is derived from the 24-oxidation pathway, possibly through the intermediate 24,25,26,27-tetranor-1,23-dihydroxyvitamin D3. The 24-oxidation pathway to calcitroic acid in bone cells is stimulated by 1,25-dihydroxyvitamin D3. The pathway in both bone cells and perfused kidney operates at physiological concentrations of substrate and appears to be capable of rapid clearance of the hormone.
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Reichel, Helmut, H. Phillip Koeffler, and Anthony W. Norman. "Regulation of 25-hydroxyvitamin D3 metabolism in a human promyelocytic leukemia cell line (HL-60): 1,25-Dihydroxyvitamin D3 stimulates the synthesis of 24,25-dihydroxyvitamin D3." Archives of Biochemistry and Biophysics 251, no. 1 (November 1986): 222–31. http://dx.doi.org/10.1016/0003-9861(86)90069-x.
Повний текст джерела
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Wang, Zhengyu, Ying Zhang, Jun Lu, Shinnshin Sun, and Katya Ravid. "Mpl Ligand Enhances the Transcription of the Cyclin D3 Gene: A Potential Role for Sp1 Transcription Factor." Blood 93, no. 12 (June 15, 1999): 4208–21. http://dx.doi.org/10.1182/blood.v93.12.4208.
Повний текст джерелаАнотація:
Abstract Cyclin D3 plays a major role in the development of polyploidy in megakaryocytes. The expression of cyclin D3 gene and the level of cyclin D3 protein are increased by the Mpl ligand in the Y10/L8057 megakaryocytic cell line, as indicated by Northern and Western blot analyses, and by nuclear run-on assays and transfection experiments with cyclin D3 promoter constructs. DNase I footprinting of the promoter region showed protected segments, at −75 to −60 bp and at −134 to −92 bp, which display binding sites for the Sp family of transcription factors. Gel mobility shift assay and supershifts with specific antibodies indicate that Sp1 binds to these regions in the cyclin D3 promoter and that Sp1 binding activity is significantly increased by Mpl ligand. Mutation of either Sp1 site both decreases the basal promoter activity and eliminates the induction by Mpl ligand. We find that the nonphosphorylated form of SP1 has greater affinity for the cyclin D3 promoter and that the majority of Sp1 in the cells is nonphosphorylated. Mpl ligand treatment results in increased levels of Sp1 protein, which also appears as nonphosphorylated. Okadaic acid, which inhibits protein phosphatase 1 (PP1) and shifts Sp1 to a phosphorylated form, decreases cyclin D3 gene expression and suppresses Mpl ligand induction. Our data point to the potential of Mpl ligand to activate at once several Sp1-dependent genes during megakaryopoiesis.
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Wang, Zhengyu, Ying Zhang, Jun Lu, Shinnshin Sun, and Katya Ravid. "Mpl Ligand Enhances the Transcription of the Cyclin D3 Gene: A Potential Role for Sp1 Transcription Factor." Blood 93, no. 12 (June 15, 1999): 4208–21. http://dx.doi.org/10.1182/blood.v93.12.4208.412k17_4208_4221.
Повний текст джерелаАнотація:
Cyclin D3 plays a major role in the development of polyploidy in megakaryocytes. The expression of cyclin D3 gene and the level of cyclin D3 protein are increased by the Mpl ligand in the Y10/L8057 megakaryocytic cell line, as indicated by Northern and Western blot analyses, and by nuclear run-on assays and transfection experiments with cyclin D3 promoter constructs. DNase I footprinting of the promoter region showed protected segments, at −75 to −60 bp and at −134 to −92 bp, which display binding sites for the Sp family of transcription factors. Gel mobility shift assay and supershifts with specific antibodies indicate that Sp1 binds to these regions in the cyclin D3 promoter and that Sp1 binding activity is significantly increased by Mpl ligand. Mutation of either Sp1 site both decreases the basal promoter activity and eliminates the induction by Mpl ligand. We find that the nonphosphorylated form of SP1 has greater affinity for the cyclin D3 promoter and that the majority of Sp1 in the cells is nonphosphorylated. Mpl ligand treatment results in increased levels of Sp1 protein, which also appears as nonphosphorylated. Okadaic acid, which inhibits protein phosphatase 1 (PP1) and shifts Sp1 to a phosphorylated form, decreases cyclin D3 gene expression and suppresses Mpl ligand induction. Our data point to the potential of Mpl ligand to activate at once several Sp1-dependent genes during megakaryopoiesis.
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Mkrtchyan, H., S. Scheler, I. Klein, A. Fahr, P. O. Couraud, I. A. Romero, B. Weksler, and T. Liehr. "Molecular Cytogenetic Characterization of the Human Cerebral Microvessel Endothelial Cell Line hCMEC/D3." Cytogenetic and Genome Research 126, no. 4 (2009): 313–17. http://dx.doi.org/10.1159/000253080.
Повний текст джерела