Browsing by Author "Dalina I. Tanyong"

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    Cytokine-induced apoptosis of beta-thalassemia/hemoglobin e erythroid progenitor cells via nitric oxide-mediated process in vitro
    (2011-11-01) Wasinee Kheansaard; Prapaporn Panichob; Suthat Fucharoen; Dalina I. Tanyong; Faculty of Medical Technology; Mahidol University
    Background/Aim: β-Thalassemia/hemoglobin E (β-thal/HbE) is a common hereditary anemia in Thailand. Ineffective erythropoiesis due to apoptosis and decreased lifespan of circulating thalassemic red blood cells are the major causes of anemia. Changes to bone marrow microenvironment could contribute to apoptotic events. This study examined the effects of cytokines interleukin-1β, tumor necrosis factor-α and interferon-γ on apoptosis of β-thal/HbE erythroid progenitor cells in vitro, including nitric oxide-mediated apoptotic processes. Methods: Percent apoptosis of erythroid progenitor cells from 5 β-thal/HbE patients and 5 normal control subjects was examined using flow cytometry. In addition, the inducible nitric oxide synthase (iNOS) mRNA level and nitrite production were measured using quantitative PCR and the Griess method, respectively. Results: Upon cytokine treatment, a higher percent apoptosis was obtained with β-thal/HbE erythroid progenitor cells compared with control, and the maximum effect was observed using 20 ng/ml interferon-γ on day 14 of culture. There was an increase in iNOS mRNA level and a concomitant elevation of nitrite concentration in culture medium. Apoptosis and nitrite level were abrogated when β-thal/HbE and control cells were treated with S-methylisothiourea sulfate, an iNOS inhibitor. Conclusion: The marked sensitivity of erythroid progenitor cells from β-thal/HbE patients to cytokine-induced apoptosis via an NO-mediated process reflects a proapoptotic status of such thalassemic red blood cells. © 2011 S. Karger AG, Basel.
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    Diallyl disulfide induces apoptosis and autophagy via mTOR pathway in myeloid leukemic cell line
    (2016-08-01) Tanitta Suangtamai; Dalina I. Tanyong; Mahidol University
    © 2016, International Society of Oncology and BioMarkers (ISOBM). Leukemia is a hematological malignancy which is produced by uncontrolled proliferation of leukocyte precursors. Currently, alternative medicines, using herb extracts, have been developed for cancer treatment. In this study, the effect of diallyl disulfide (DADS) on the induction of apoptosis and autophagy was investigated in K562 and NB4 myeloid leukemia cells. Leukemia cells were treated with various concentrations of DADS for 24 and 48 h. The percentage of cell viability was measured using an MTT assay. The percentages of apoptosis and autophagy were analyzed by staining with annexin-FITC and anti-LC3 FITC-conjugated antibodies, respectively. Then, the stained cells were detected by flow cytometry. In addition, PP242, a mammalian target rapamycin (mTOR) inhibitor, was used to study the involvement of the mTOR pathway in DADS-induced apoptosis and autophagy. mTOR mRNA expression was measured by real-time PCR. The results showed that DADS decreased cell viability and increased the percentage of cell apoptosis in a dose- and time-dependent manner. mTOR expression was significantly decreased in DADS- and mTOR inhibitor-treated cells. The highest percentages of apoptosis and autophagy were shown in cells treated with 100 μg/ml DADS combined with 10 μM of the mTOR inhibitor. According to our results, DADS could induce apoptosis and autophagy via the mTOR pathway in both K562 and NB4 myeloid leukemia cell lines.
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    Effect of tumor necrosis factor-alpha on erythropoietinand erythropoietin receptor-induced erythroid progenitor cell proliferation in β-Thalassemia/Hemoglobin e patients
    (2015-01-01) Dalina I. Tanyong; Prapaporn Panichob; Wasinee Kheansaard; Suthat Fucharoen; Mahidol University
    © 2015 Turkish Society of Hematology. All rights reserved. Objective: Thalassemia is one of the genetic diseases that cause anemia and ineffective erythropoiesis. Increased levels of several inflammatory cytokines have been reported in β-thalassemia and might contribute to ineffective erythropoiesis. However, the mechanism by which tumor necrosis factor-alpha (TNF-α) is involved in ineffective erythropoiesis in thalassemic patients remains unclear. The objective of this study is to investigate the effect of TNF-α on the erythropoietin (EPO) and erythropoietin receptor (EPOR) expression involved in proliferation of β-thalassemia/hemoglobin (Hb) E erythroid progenitor cells compared with cells from healthy subjects. Materials and Methods: CD34-positive cells were isolated from heparinized blood by using the EasySep® CD34 selection kit. Cells were then cultured with suitable culture medium in various concentrations of EPO for 14 days. The effect of TNF-α on percent cell viability was analyzed by trypan blue staining. In addition, the percentage of apoptosis and levels of EPOR protein were measured by flow cytometry. Results: Upon EPO treatment, a higher cell number was observed for erythroid progenitor cells from both healthy participants and β-thalassemia/Hb E patients. However, a reduction of apoptosis was found in EPO-treated cells especially for β-thalassemia/ Hb E patients. Interestingly, TNF-α caused higher levels of cell apoptosis and lower levels of EPOR protein in thalassemic erythroid progenitor cells. Conclusion: TNF-α caused a reduction in the level of EPOR protein and EPO-induced erythroid progenitor cell proliferation. It is possible that TNF-α could be involved in the mechanism of ineffective erythropoiesis in β-thalassemia/Hb E patients.
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    Interferon-gamma induced nitric oxide-mediated apoptosis of anemia of chronic disease in rheumatoid arthritis
    (2013-01-01) Wasinee Kheansaard; Sumana Mas-Oo-Di; Surasak Nilganuwong; Dalina I. Tanyong; Mahidol University
    Proinflammatory cytokines play a role in the pathogenesis of anemia of chronic disease (ACD), which is a common cause of anemia in rheumatoid arthritis (RA). Anemia in RA is associated with increased apoptosis of erythroid cells. However, there is unclear information on the mechanism of ACD in the disease. The purpose of this study is to investigate the role of cytokines on nitric oxide-mediated apoptosis in erythroid progenitor cells of ACD in RA patients. Erythroid progenitor cells from healthy subjects and RA patients with ACD were treated with cytokines like interleukin-1β, tumor necrosis factor-α, and interferon-γ at concentrations of 2, 20, and 40 ng/ml for 14 days. Cell viability and cell apoptosis were analyzed by trypan blue staining and flow cytometry, respectively. The results showed that the highest effect of cytokines on reduction cell viability and induction cell apoptosis was found in 20 ng/ml IFN-γ-treated cells of RA patients. In addition, IFN-γ showed significantly increased nitric oxide production and iNOS mRNA expression, which was measured by Griess assay and real-time PCR, respectively. The percentage of cell apoptosis and NO production was reduced after an inducible nitric oxide synthase inhibitor, SMT, treatment. In conclusion, IFN-γ could induce nitric oxide production-mediated apoptosis process, which might be involved in the pathogenesis of ACD in RA patients. © 2012 Springer-Verlag.
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    Nitric oxide and caspase 3 mediated cytokine inducedapoptosis in acute leukemia
    (2011-03-01) Darin Siripin; Suthat Fucharoen; Dalina I. Tanyong; Mahidol University
    Background: Leukemia is characterized by theuncontrolled accumulation of white blood cells.Recently, cytokines have been used inimmunotherapy, which is a new strategy forleukemia treatment.Objective: To investigate the effect of cytokineson induction of apoptosis in acute leukemic celllines; HL-60, MV4-11, K-562 and Molt-4 andin addition, to study the involvement of nitricoxide (NO) in apoptotic pathways.Methods: Leukemic cell lines were incubatedwith cytokines; interleukin-1β, tumor necrosis factor-α, and interferon-γ in variousconcentrations and for variable periods oftime. The percent apoptosis and caspase 3activation were examined by flow cytometry.Moreover, NO production and inducible nitricoxide synthase (iNOS) mRNA were measuredby using Griess method and Real-time PCR,respectively.Results: Cytokines caused a time and dosedependentinduction of apoptosis in leukemiccell lines. The highest cell apoptosis was foundin K-562 treated with 40 U/ml interferon-γ for48 hours; this correlated with the result of cellgrowth inhibition and caspase 3 activation. NOand iNOS mRNA were increased in cytokinestreated cells. Moreover, apoptosis was reducedby SMT, an iNOS inhibitor, which confirmsthe possible involvement of NO in the apoptoticpathway.Conclusion: Cytokines especially interferon-γ induced apoptosis in acute leukemia via NOand caspase 3 pathway.
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    P53 and nitric oxide are involved in cytokine-induced apoptosis in Kasumi-1 and Molt-4 Leukemics cells
    (2014-01-01) Aishath Maharath; Suthat Fucharoen; Dalina I. Tanyong; Mahidol University
    Background: Immunotherapy has been developed to treat cancers. There are many signaling pathways involved in cytokine induced apoptosis of many cancers but their role remains unclear in some cancers such as leukemia. Objective: To investigate the involvement of the nitric oxide (NO) and p53 tumor suppressor gene in apoptotic pathways induced by cytokines in leukemic cell lines. Methods: Leukemic cell lines, Kasumi-1 (AMLM2) and Molt- 4 (ALL) were treated with cytokines, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ). The effect of cytokines on the induction cell apoptosis was analysed by flow cytometry. In addition, nitric oxide production and p53 protein levels were measured by using the Griess method and Western blot, respectively. Results: Upon cytokine treatment, there was a significant increase in the percentage of cell apoptosis in both leukemic cell lines. The highest apoptosis was shown in 40 U/ml IFN-γ treated cells. In addition, nitric oxide and p53 protein increased in IFN-γ treated cells. There was a reduction of apoptosis and p53 level after adding the inducible nitric oxide synthase inhibitor, SMT. Conclusion: P53 and nitric oxide are involved in the mediation of apoptosis induced by cytokines in Kasumi-1 and Molt-4 leukemic cell lines.
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    Role of interleukin-3 and signaling pathways on β-thalassemia/HbE erythroid progenitor cell in culture
    (2007-09-01) Dalina I. Tanyong; Pranee Winichagoon; Darin Siripin; Weerayut Seevakool; Suthat Fucharoen; Mahidol University; The Institute of Science and Technology for Research and Development, Mahidol University
    In order to study the role of the cytokine interleukin-3 (IL-3) and its signaling pathways in erythropoiesis of β-thalassemia/HbE erythroid progenitor cells, CD34 positive cells were isolated from peripheral blood of patients and healthy subjects. After culturing the cells in the presence or absence of IL-3, cell viability was measured by trypan blue staining and apoptotic cells were analyzed by flow cytometry. After 7 days of culture the highest percent erythroid progenitor cell viability was obtained with cells from healthy subjects, while the lowest percentage was found in those from splenectomized β-thalassemia/HbE. Viability of β-thalassemia/HbE erythroid progenitor cells in the presence of IL-3 was higher than that of nonsupplemented cells. In addition, specific inhibitors of protein kinase C (Ro-318220), phospholipase C (U-73122) and Janus kinase 2 (AG-490) were used to investigate the involvement of signaling pathways in erythropoiesis. Percent apoptosis of erythroid progenitor cells from splenectomized β-thalassemia/ HbE subjects treated with RO-318220 was higher than those of nonsplenectomized β-thalassemia/HbE and healthy subjects. Treatment with U-73122 resulted in enhanced percent apoptotic cells from normal and β-thalassemia/HbE subjects. All these effects were independent of IL-3 treatment.