The Experts below are selected from a list of 261 Experts worldwide ranked by ideXlab platform
Jerry J. Warsh - One of the best experts on this subject based on the ideXlab platform.
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CACNA1C SNP rs1006737 associates with Bipolar I disorder independent of the Bcl-2 SNP rs956572 variant and its associated effect on intracellular calcium homeostasis
2016Co-Authors: Takuji Uemura, Marty Green, Jerry J. WarshAbstract:OBjectives. Intracellular calcium (Ca2+) dyshomeostasis (ICDH) has Been implicated in Bipolar disorder (BD) pathophysiology. We previously showed that SNP rs956572 in the B-cell CLL/lymphoma 2 (Bcl-2) gene associates with elevated B lymphoBlast (BLCL) intracellular Ca2+ concentrations ([Ca2+]B) differentially in BD-I. Genome-wide association studies strongly support the association Between BD and the SNP rs1006737, located within the L-type voltage-dependent Ca2+ channel α1C suBunit gene (CACNA1C). Here we investigated whether this CACNA1C variant also associates with ICDH and interacts with SNP rs956572 on [Ca2+]B in BD-I. Methods. CACNA1C SNP rs1006737 was genotyped in 150 BD-I, 65 BD-II, 30 major depressive disorder patients, and 70 healthy suBjects with availaBle BLCL [Ca2+]B and Bcl-2 SNP rs956572 genotype measures. Results. SNP rs1006737 was significantly associated with BD-I. The [Ca2+]B was significantly higher in BD-I rs1006737 A compared with healthy A allele carriers and also in healthy GG compared with A allele carriers. There was no significant interaction Between SNP rs1006737 and SNP rs956572 on [Ca2+]B. Conclusions. Our study further supports the association of SNP rs1006737 with BD-I and suggests that CACNA1C SNP rs1006737 and Bcl-2 SNP rs956572, or specific causal variants in LD with these proxies, act independently to increase risk and ICDH in BD-I.
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Effect of oxidative stress on TRPM2 and TRPC3 channels in B lymphoBlast cells in Bipolar disorder.
Bipolar disorders, 2012Co-Authors: Angela S. Roedding, Andrew F Gao, Wynne Au-yeung, Tiffany Scarcelli, Jerry J. WarshAbstract:Roedding AS, Gao AF, Au-Yeung W, Scarcelli T, Li PP, Warsh JJ. Effect of oxidative stress on TRPM2 and TRPC3 channels in B lymphoBlast cells in Bipolar disorder. Bipolar Disord 2012: 14: 151–161. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. OBjectives: Recent findings implicate the calcium-permeaBle nonselective ion channels transient receptor potential (TRP) melastatin suBtype 2 (TRPM2) and canonical suBtype 3 (TRPC3) in the pathogenesis of Bipolar disorder (BD). These channels are involved in calcium and oxidative stress signaling, Both of which are disrupted in BD. Thus, we sought to determine if these channels are differentially affected By oxidative stress in cell lines of BD patient origin. Methods: B lymphoBlast cell lines (BLCLs) from Bipolar I disorder (BD-I) patients (n = 6) and healthy controls (n = 5) were challenged with the oxidative stressor rotenone (2.5 μM and 10 μM) or vehicle for acute (24 hours) and chronic (four days) intervals. Cell viaBility was measured using propidium iodide, while TRPM2- and TRPC3-mediated calcium fluxes were measured in the presence of their respective activators (H2O2 and 1-oleoyl-2-acetyl-sn-glycerol) using Fluo-4. Changes in TRPM2 and TRPC3 expression levels were determined By quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western Blotting. Results: Cell viaBility decreased with increasing dose and duration of rotenone treatment, with BD-I patient BLCLs more susceptiBle than controls acutely (p
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effect of oxidative stress on trpm2 and trpc3 channels in B lymphoBlast cells in Bipolar disorder
Bipolar Disorders, 2012Co-Authors: Angela S. Roedding, Andrew F Gao, Tiffany Scarcelli, Wynne Auyeung, Jerry J. WarshAbstract:Roedding AS, Gao AF, Au-Yeung W, Scarcelli T, Li PP, Warsh JJ. Effect of oxidative stress on TRPM2 and TRPC3 channels in B lymphoBlast cells in Bipolar disorder. Bipolar Disord 2012: 14: 151–161. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. OBjectives: Recent findings implicate the calcium-permeaBle nonselective ion channels transient receptor potential (TRP) melastatin suBtype 2 (TRPM2) and canonical suBtype 3 (TRPC3) in the pathogenesis of Bipolar disorder (BD). These channels are involved in calcium and oxidative stress signaling, Both of which are disrupted in BD. Thus, we sought to determine if these channels are differentially affected By oxidative stress in cell lines of BD patient origin. Methods: B lymphoBlast cell lines (BLCLs) from Bipolar I disorder (BD-I) patients (n = 6) and healthy controls (n = 5) were challenged with the oxidative stressor rotenone (2.5 μM and 10 μM) or vehicle for acute (24 hours) and chronic (four days) intervals. Cell viaBility was measured using propidium iodide, while TRPM2- and TRPC3-mediated calcium fluxes were measured in the presence of their respective activators (H2O2 and 1-oleoyl-2-acetyl-sn-glycerol) using Fluo-4. Changes in TRPM2 and TRPC3 expression levels were determined By quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western Blotting. Results: Cell viaBility decreased with increasing dose and duration of rotenone treatment, with BD-I patient BLCLs more susceptiBle than controls acutely (p < 0.001). A dose-dependent decrease in TRPC3 protein expression occurred after chronic (24%, p = 0.008) But not acute rotenone treatment. Interestingly, H2O2-provoked TRPM2-dependent calcium fluxes revealed an interaction Between the effects of stressor addition and diagnostic suBject group (p = 0.003). Conclusions: These data support an important role for TRPM2 and TRPC3 in sensing and responding to oxidative stress and in transducing oxidative stress signaling to intracellular calcium homeostasis and cellular stress responses, all of which have Been implicated in the pathophysiology of BD.
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Differential modulation of intracellular Ca2+ responses in B lymphoBlasts By mood staBilizers.
The international journal of neuropsychopharmacology, 2009Co-Authors: Tatiana Perova, Melodie Kwan, Jerry J. WarshAbstract:Irregularities of intracellular calcium (Ca2+) homeostasis have Been implicated in the pathophysiology of Bipolar disorder (BD). Findings that chronic ex-vivo treatment with lithium modifies lysophosphatidic acid (LPA)-stimulated Ca2+ responses in B lymphoBlast cell lines (BLCLs) from BD-I patients and healthy controls, and differentially decreases levels of the type-3 canonical transient receptor potential Ca2+-permeaBle channel in BLCLs from BD-I patients, support the view that the amelioration of these aBnormalities is important in the therapeutic action of lithium. To determine whether other clinically efficacious mood staBilizers share these effects, LPA (100 mum)- and thapsigargin (TG, 200 nm)-stimulated Ca2+ responses were determined in BLCLs from BD-I patients and healthy controls treated acutely (24 h) and chronically (7 d) ex vivo with therapeutically relevant concentrations of lithium (0.75 mm), valproate (0.5 mm), lamotrigine (15 mum) or respective vehicles. Chronic treatment with valproate significantly attenuated LPA-stimulated Ca2+ responses ([downward arrow]8%: F's=9.1-9.4, d.f.=1, 9, p's
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Hyperactive intracellular calcium dynamics in B lymphoBlasts from patients with Bipolar I disorder
The international journal of neuropsychopharmacology, 2007Co-Authors: Tatiana Perova, Michael J Wasserman, Jerry J. WarshAbstract:SuBstantial evidence implicates aBnormalities of intracellular calcium (Ca2+) dynamics in the pathophysiology of Bipolar disorder (BD). However, the precise mechanisms underlying such disturBances are poorly understood. To further elaBorate the nature of altered intracellular Ca2+ signalling dynamics that occur in BD, we examined receptor- and store-operated Ca2+ responses in B lymphoBlast cell lines (BLCLs), which have Been found in earlier studies to 'report' BD-associated disturBances. Basal Ca2+ concentrations ([Ca2+]B), and lysophosphatidic acid (LPA)- and thapsigargin-stimulated Ca2+ responses were determined in BLCLs from 52 BD-I patients and 30 healthy comparison suBjects using fura-2, and ratiometric fluorometry. ANOVA revealed a significant effect of diagnosis, But not gender, on [Ca2+]B (F1,63=4.4, p=0.04) and the rate of rise (F1,63=5.2, p=0.03) of LPA-stimulated Ca2+ responses in BLCLs from patients compared with those from healthy suBjects. A significant genderxdiagnosis interaction on the LPA-induced rate of rise (F1,63=4.6, p=0.03) was accounted for By a faster rate of rise (97%) in BLCLs from BD-I males compared with healthy males But not in those from female patients compared with healthy females. A genderxdiagnosis interaction in thapsigargin-evoked Ca2+ influx (F1,61=3.8, p=0.05) resulted from a significantly higher peak [Ca2+]influx (24%) in BLCLs from female compared with male patients. The results suggest more rapid LPA-stimulated Ca2+ responses occur in BLCLs from BD-I patients compared with controls, which are proBaBly mediated, in part, By canonical transient receptor potential type 3 (TRPC3)-like channels. Additionally, this study highlights sex-dependent differences that can occur in the pathophysiological disturBances involved in BD.
Chunlin Shao - One of the best experts on this subject based on the ideXlab platform.
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Role of DNA methylation in the adaptive responses induced in a human B lymphoBlast cell line By long-term low-dose exposures to γ-rays and cadmium
Mutation research. Genetic toxicology and environmental mutagenesis, 2014Co-Authors: Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:ABstract The possiBle involvement of epigenetic factors in health risks due to exposures to environmental toxicants and ionizing radiation is poorly understood. We have tested the hypothesis that DNA methylation contriButes to the adaptive response (AR) to ionizing radiation or Cd. Human B lymphoBlast cells HMy2.CIR were irradiated (0.032 Gy γ-rays) three times per week for 4 weeks or exposed to CdCl 2 (0.005, 0.01, or 0.1 μM) for 3 months, and then challenged with a high dose of Cd (50 or 100 μM) or γ-rays (2 Gy). Long-term low-dose radiation (LDR) or long-term low-dose Cd exposure induced AR against challenging doses of Cd and irradiation, respectively. When the primed cells were treated with 5-aza-2′-deoxycytidine (5-aza-dC), a DNA methyltransferase inhiBitor, the ARs were eliminated. These results indicate that DNA methylation is involved in the induction of AR in HMy2.CIR cells.
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Simulated microgravity increases heavy ion radiation-induced apoptosis in human B lymphoBlasts
Life sciences, 2013Co-Authors: Bingrong Dang, Yuping Yang, Erdong Zhang, Yue Meng, Siqi Yan, Zhuanzi Wang, Wei Wei, Chunlin ShaoAbstract:Microgravity and radiation, common in space, are the main factors influencing astronauts' health in space flight, But their comBined effects on immune cells are extremely limited. Therefore, the effect of simulated microgravity on heavy ion radiation-induced apoptosis, and reactive oxygen species (ROS)-sensitive apoptosis signaling were investigated in human B lymphoBlast HMy2.CIR cells. Simulated microgravity was achieved using a Rotating Wall Vessel Bioreactor at 37°C for 30 min. Heavy carBon-ion irradiation was carried out at 300 MeV/u, with a linear energy transfer (LET) value of 30 keV/μm and a dose rate of 1Gy/min. Cell survival was evaluated using the Trypan Blue exclusion assay. Apoptosis was indicated By Annexin V/propidium iodide staining. ROS production was assessed By cytometry with a fluorescent proBe dichlorofluorescein. Malondialdehyde was detected using a kit. Extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase phosphatase-1 (MKP-1) and caspase-3 activation were measured By immunoBlotting. Simulated microgravity decreased heavy ion radiation-induced cell survival and increased apoptosis in HMy2.CIR cells. It also amplified heavy ion radiation-elicited intracellular ROS generation, which induced ROS-sensitive ERK/MKP-1/caspase-3 activation in HMy2.CIR cells. The aBove phenomena could Be reversed By the antioxidants N-acetyl cysteine (NAC) and quercetin. These results illustrated that simulated microgravity increased heavy ion radiation-induced cell apoptosis, mediated By a ROS-sensitive signal pathway in human B lymphoBlasts. Further, the antioxidants NAC and quercetin, especially NAC, might Be good candidate drugs for protecting astronauts' and space travelers' health and safety. Copyright © 2013 Elsevier Inc. All rights reserved.
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Role of DNA methylation in long-term low-dose γ-rays induced adaptive response in human B lymphoBlast cells.
International journal of radiation biology, 2013Co-Authors: Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:ABstractPurpose: With widespread use of ionizing radiation, more attention has Been attracted to low-dose radiation (LDR); however, the mechanisms of long-term LDR-induced Bio-effects are unclear. Here, we applied human B lymphoBlast cell line HMy2.CIR to monitor the effects of long-term LDR and the potential involvement of DNA methylation.Materials and methods: HMy2.CIR cells were irradiated with 0.032 Gy γ-rays three times per week for 1–4 weeks. Some of these primed cells were further challenged with 2 Gy γ-rays. Cell proliferation, micronuclei formation, gene expression of DNA methyltransferases (DNMT), levels of gloBal genomic DNA methylation and protein expression of methyl CpG Binding protein 2 (MeCP2) and heterochromatin protein-1 (HP1) were measured.Results: Long-term LDR enhanced cell proliferation and clonogenicity and triggered a cellular adaptive response (AR). Furthermore, gloBal genomic DNA methylation was increased in HMy2.CIR cells after long-term LDR, accompanied with an increase of gene...
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Role of DNA methylation in long-term low-dose γ-rays induced adaptive response in human B lymphoBlast cells.
International journal of radiation biology, 2013Co-Authors: Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:With widespread use of ionizing radiation, more attention has Been attracted to low-dose radiation (LDR); however, the mechanisms of long-term LDR-induced Bio-effects are unclear. Here, we applied human B lymphoBlast cell line HMy2.CIR to monitor the effects of long-term LDR and the potential involvement of DNA methylation. HMy2.CIR cells were irradiated with 0.032 Gy γ-rays three times per week for 1-4 weeks. Some of these primed cells were further challenged with 2 Gy γ-rays. Cell proliferation, micronuclei formation, gene expression of DNA methyltransferases (DNMT), levels of gloBal genomic DNA methylation and protein expression of methyl CpG Binding protein 2 (MeCP2) and heterochromatin protein-1 (HP1) were measured. Long-term LDR enhanced cell proliferation and clonogenicity and triggered a cellular adaptive response (AR). Furthermore, gloBal genomic DNA methylation was increased in HMy2.CIR cells after long-term LDR, accompanied with an increase of gene expression of DNMT1 and protein expression of MeCP2 and HP1. After treatment with 5-aza-2'-deoxycytidine (5-aza-dC), a DNA methyltransferase inhiBitor, the long-term LDR-induced gloBal genomic DNA hypermethylation was decreased and the AR was eliminated. GloBal genomic DNA hypermethylation accompanied with increases of DNMT1 and MeCP2 expression and heterochromatin formation might Be involved in long-term LDR-induced adaptive response.
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effects of long term low dose γ rays exposure on radiosensitivity of human B lymphoBlast cells
Chinese journal of radiological medicine and protection, 2013Co-Authors: Y E Shuang, Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:OBjective To investigate the effects of long-term low-dose radiation (LDR) of γ-rays on the proliferation and radiosensitivity of human lymphoBlast cells HMy2.CIR (HMy) and to elucidate the underlying mechanism.Methods HMy cells were divided into control group and long-term LDR group.For the long-term LDR treatment,HMy cells were fractionally exposed to a low dose of γ-rays,which could enhance cell proliferation,3 times per week for 4 weeks.After the long-term LDR exposure,part of the control and long-term LDR exposed cells were further irradiated with a challenging dose (2 Gy) of γ-rays.Then cell proliferation and radiosensitivity were assayed By CCK-8 kit,cell apoptosis,and γ-H2AX formation was measured By flow cytometry.Gene expressions of cyclinD1,PCNA,Bcl-2 and Bax were detected By RT-PCR.Results The long-term LDR significantly increased cell proliferation (t =9.607,P ＜ 0.01) accompanied with up-regulation of cell cycle regulation gene cyclinD1 (t =6.869,P ＜ 0.01),proliferation regulation gene PCNA (proliferating cell nuclear antigen) (t =9.229,P ＜ 0.01) and Bcl-2 gene (t =2.662,P ＜ 0.05),But decreased the expression of pro-apoptotic gene Bax (t =19.908,P ＜0.01) in HMy cells.Compared to untreated cells,the long-term LDR decreased cell radiosensitivity (t =8.896,P ＜ 0.01),including apoptosis induction (t =4.762,P ＜ 0.01) and γ-H2AX formation (t =10.264,P＜0.01).Conclusions The long-term LDR promoted cell proliferation By up-regulating cell cycle related genes,while it reduced the radiosensitivity of HMy cells with acquisition of apoptotic resistance. Key words: Low-dose-radiation ; Cell proliferation ; Radiosensitivity ; Apoptosis ; Gene expressions
Angela S. Roedding - One of the best experts on this subject based on the ideXlab platform.
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Effect of oxidative stress on TRPM2 and TRPC3 channels in B lymphoBlast cells in Bipolar disorder.
Bipolar disorders, 2012Co-Authors: Angela S. Roedding, Andrew F Gao, Wynne Au-yeung, Tiffany Scarcelli, Jerry J. WarshAbstract:Roedding AS, Gao AF, Au-Yeung W, Scarcelli T, Li PP, Warsh JJ. Effect of oxidative stress on TRPM2 and TRPC3 channels in B lymphoBlast cells in Bipolar disorder. Bipolar Disord 2012: 14: 151–161. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. OBjectives: Recent findings implicate the calcium-permeaBle nonselective ion channels transient receptor potential (TRP) melastatin suBtype 2 (TRPM2) and canonical suBtype 3 (TRPC3) in the pathogenesis of Bipolar disorder (BD). These channels are involved in calcium and oxidative stress signaling, Both of which are disrupted in BD. Thus, we sought to determine if these channels are differentially affected By oxidative stress in cell lines of BD patient origin. Methods: B lymphoBlast cell lines (BLCLs) from Bipolar I disorder (BD-I) patients (n = 6) and healthy controls (n = 5) were challenged with the oxidative stressor rotenone (2.5 μM and 10 μM) or vehicle for acute (24 hours) and chronic (four days) intervals. Cell viaBility was measured using propidium iodide, while TRPM2- and TRPC3-mediated calcium fluxes were measured in the presence of their respective activators (H2O2 and 1-oleoyl-2-acetyl-sn-glycerol) using Fluo-4. Changes in TRPM2 and TRPC3 expression levels were determined By quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western Blotting. Results: Cell viaBility decreased with increasing dose and duration of rotenone treatment, with BD-I patient BLCLs more susceptiBle than controls acutely (p
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effect of oxidative stress on trpm2 and trpc3 channels in B lymphoBlast cells in Bipolar disorder
Bipolar Disorders, 2012Co-Authors: Angela S. Roedding, Andrew F Gao, Tiffany Scarcelli, Wynne Auyeung, Jerry J. WarshAbstract:Roedding AS, Gao AF, Au-Yeung W, Scarcelli T, Li PP, Warsh JJ. Effect of oxidative stress on TRPM2 and TRPC3 channels in B lymphoBlast cells in Bipolar disorder. Bipolar Disord 2012: 14: 151–161. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. OBjectives: Recent findings implicate the calcium-permeaBle nonselective ion channels transient receptor potential (TRP) melastatin suBtype 2 (TRPM2) and canonical suBtype 3 (TRPC3) in the pathogenesis of Bipolar disorder (BD). These channels are involved in calcium and oxidative stress signaling, Both of which are disrupted in BD. Thus, we sought to determine if these channels are differentially affected By oxidative stress in cell lines of BD patient origin. Methods: B lymphoBlast cell lines (BLCLs) from Bipolar I disorder (BD-I) patients (n = 6) and healthy controls (n = 5) were challenged with the oxidative stressor rotenone (2.5 μM and 10 μM) or vehicle for acute (24 hours) and chronic (four days) intervals. Cell viaBility was measured using propidium iodide, while TRPM2- and TRPC3-mediated calcium fluxes were measured in the presence of their respective activators (H2O2 and 1-oleoyl-2-acetyl-sn-glycerol) using Fluo-4. Changes in TRPM2 and TRPC3 expression levels were determined By quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western Blotting. Results: Cell viaBility decreased with increasing dose and duration of rotenone treatment, with BD-I patient BLCLs more susceptiBle than controls acutely (p < 0.001). A dose-dependent decrease in TRPC3 protein expression occurred after chronic (24%, p = 0.008) But not acute rotenone treatment. Interestingly, H2O2-provoked TRPM2-dependent calcium fluxes revealed an interaction Between the effects of stressor addition and diagnostic suBject group (p = 0.003). Conclusions: These data support an important role for TRPM2 and TRPC3 in sensing and responding to oxidative stress and in transducing oxidative stress signaling to intracellular calcium homeostasis and cellular stress responses, all of which have Been implicated in the pathophysiology of BD.
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Characterization of the transient receptor potential channels mediating lysophosphatidic acid-stimulated calcium moBilization in B lymphoBlasts.
Life sciences, 2006Co-Authors: Angela S. Roedding, Jerry J. WarshAbstract:Altered 1-oleoyl-lysophosphatidic acid (LPA, 100 microM)-stimulated calcium responses occur in B-lymphoBlast cell lines from Bipolar disorder patients, But the mechanism(s) involved is uncertain. Lysophosphatidic acid shares a structurally similar fatty acid side chain with the diacylglycerol analogue, 1-oleoyl-2-acetyl-sn-glycerol (OAG), a known activator of suBtypes 3, 6 and 7 of the canonical transient receptor potential (TRPC) cation channel suBfamily. Accordingly, the oBjective of this study was to determine whether the LPA-stimulated calcium response in B-lymphoBlasts is mediated, in part, through this TRPC channel suBfamily. Divalent cation selectivity in response to thapsigargin, LPA and OAG were used to distinguish TRPC-like character of the responses to these agents in BLCLs. The sensitivity to gadolinium, an inhiBitor of capacitative calcium channels, was used to determine the store-operated nature of the responses. The TRPC isoforms that are present in BLCLs as identified By immunoBlotting and/or PCR include TRPC1, 3 and 5. Minimal Barium influx in calcium-free Buffer was oBserved following thapsigargin stimulation. However, LPA stimulated Barium influx of a magnitude similar to that induced By OAG. Thapsigargin-provoked calcium influx was completely inhiBited By gadolinium (10 microM), whereas LPA and OAG-stimulated responses were partially inhiBited and potentiated, respectively. The results suggest that 100 microM LPA stimulates calcium entry through channels with characteristics similar to TRPC3, as TRPC6 and 7 are aBsent in B-lymphoBlasts.
Meibian Zhang - One of the best experts on this subject based on the ideXlab platform.
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Studying the genotoxic effects induced By two kinds of Bentonite particles on human B lymphoBlast cells in vitro.
Mutation research, 2011Co-Authors: Meibian Zhang, Qing Chen, Xinglin Fang, Mingluan XingAbstract:The aim of the present study was to evaluate the genotoxic effects induced By native and active Bentonite particles (BPs) on human B lymphoBlast cells using comet assay and cytokinesis-Block micronucleus (CBMN) assay in vitro. The cells were exposed to BPs at the concentrations of 30, 60, 120 and 240μg/ml for 24, 48 and 72h, respectively. The quartz contents of native and active BPs were 6.80±0.20 and 6.50±0.10%, respectively. Gypsum and DQ-12 quartz served as negative and positive controls. The results of comet assay showed that DNA damage induced By native and active BPs was significantly higher than that induced By gypsum control (P
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studying the cytotoxicity and oxidative stress induced By two kinds of Bentonite particles on human B lymphoBlast cells in vitro
Chemico-Biological Interactions, 2010Co-Authors: Meibian Zhang, Qing Chen, Mingluan Xing, Hua ZouAbstract:The aim of the present study was to evaluate the cytotoxicity and oxidative stress induced By native and active Bentonite particles (BPs) on human B lymphoBlast cells using seven assays. Our results showed that the order of cytotoxicity was: active BPs > native BPs > quartz particles (DQ-12) > gypsum, according to the IC50 values in CCK-8 assay and neutral red uptake (NRU) assay. The lactate dehydrogenase (LDH) leakage, the proportions of early apoptotic cells, the reactive oxygen species (ROS) generation, the superoxide dismutase (SOD) inhiBition and the malondialdehyde (MDA) release in the native and active BPs groups were significantly higher than those in the gypsum and DQ-12 groups (P < 0.05 or P < 0.01). Moreover, the cytotoxicity of active BPs with higher adsorption capacity of phenol was higher than that of native BPs with relatively lower adsorption capacity of phenol. The oxidative stress induced By active BPs was significantly higher than that induced By native BPs (P < 0.05 or P < 0.01). The water-soluBle fractions of BPs did not induce the cytotoxicity and ROS generation. These findings indicated that active and native BPs could induce significantly the cytotoxic effects and oxidative stress on human B lymphoBlast cells in vitro. The cytotoxic difference Between active BPs and native BPs may Be associated with the adsorption capacity of BPs and oxidative stress induced By BPs to a certain extent. The insoluBle particle fractions may play a main role in the cytotoxic effects and oxidative stress induced By BPs.
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Studying the cytotoxicity and oxidative stress induced By two kinds of Bentonite particles on human B lymphoBlast cells in vitro
Chemico-biological interactions, 2009Co-Authors: Meibian Zhang, Qing Chen, Mingluan Xing, Hua ZouAbstract:The aim of the present study was to evaluate the cytotoxicity and oxidative stress induced By native and active Bentonite particles (BPs) on human B lymphoBlast cells using seven assays. Our results showed that the order of cytotoxicity was: active BPs > native BPs > quartz particles (DQ-12) > gypsum, according to the IC50 values in CCK-8 assay and neutral red uptake (NRU) assay. The lactate dehydrogenase (LDH) leakage, the proportions of early apoptotic cells, the reactive oxygen species (ROS) generation, the superoxide dismutase (SOD) inhiBition and the malondialdehyde (MDA) release in the native and active BPs groups were significantly higher than those in the gypsum and DQ-12 groups (P
Dexiao Yuan - One of the best experts on this subject based on the ideXlab platform.
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Role of DNA methylation in the adaptive responses induced in a human B lymphoBlast cell line By long-term low-dose exposures to γ-rays and cadmium
Mutation research. Genetic toxicology and environmental mutagenesis, 2014Co-Authors: Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:ABstract The possiBle involvement of epigenetic factors in health risks due to exposures to environmental toxicants and ionizing radiation is poorly understood. We have tested the hypothesis that DNA methylation contriButes to the adaptive response (AR) to ionizing radiation or Cd. Human B lymphoBlast cells HMy2.CIR were irradiated (0.032 Gy γ-rays) three times per week for 4 weeks or exposed to CdCl 2 (0.005, 0.01, or 0.1 μM) for 3 months, and then challenged with a high dose of Cd (50 or 100 μM) or γ-rays (2 Gy). Long-term low-dose radiation (LDR) or long-term low-dose Cd exposure induced AR against challenging doses of Cd and irradiation, respectively. When the primed cells were treated with 5-aza-2′-deoxycytidine (5-aza-dC), a DNA methyltransferase inhiBitor, the ARs were eliminated. These results indicate that DNA methylation is involved in the induction of AR in HMy2.CIR cells.
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Role of DNA methylation in long-term low-dose γ-rays induced adaptive response in human B lymphoBlast cells.
International journal of radiation biology, 2013Co-Authors: Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:ABstractPurpose: With widespread use of ionizing radiation, more attention has Been attracted to low-dose radiation (LDR); however, the mechanisms of long-term LDR-induced Bio-effects are unclear. Here, we applied human B lymphoBlast cell line HMy2.CIR to monitor the effects of long-term LDR and the potential involvement of DNA methylation.Materials and methods: HMy2.CIR cells were irradiated with 0.032 Gy γ-rays three times per week for 1–4 weeks. Some of these primed cells were further challenged with 2 Gy γ-rays. Cell proliferation, micronuclei formation, gene expression of DNA methyltransferases (DNMT), levels of gloBal genomic DNA methylation and protein expression of methyl CpG Binding protein 2 (MeCP2) and heterochromatin protein-1 (HP1) were measured.Results: Long-term LDR enhanced cell proliferation and clonogenicity and triggered a cellular adaptive response (AR). Furthermore, gloBal genomic DNA methylation was increased in HMy2.CIR cells after long-term LDR, accompanied with an increase of gene...
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Role of DNA methylation in long-term low-dose γ-rays induced adaptive response in human B lymphoBlast cells.
International journal of radiation biology, 2013Co-Authors: Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:With widespread use of ionizing radiation, more attention has Been attracted to low-dose radiation (LDR); however, the mechanisms of long-term LDR-induced Bio-effects are unclear. Here, we applied human B lymphoBlast cell line HMy2.CIR to monitor the effects of long-term LDR and the potential involvement of DNA methylation. HMy2.CIR cells were irradiated with 0.032 Gy γ-rays three times per week for 1-4 weeks. Some of these primed cells were further challenged with 2 Gy γ-rays. Cell proliferation, micronuclei formation, gene expression of DNA methyltransferases (DNMT), levels of gloBal genomic DNA methylation and protein expression of methyl CpG Binding protein 2 (MeCP2) and heterochromatin protein-1 (HP1) were measured. Long-term LDR enhanced cell proliferation and clonogenicity and triggered a cellular adaptive response (AR). Furthermore, gloBal genomic DNA methylation was increased in HMy2.CIR cells after long-term LDR, accompanied with an increase of gene expression of DNMT1 and protein expression of MeCP2 and HP1. After treatment with 5-aza-2'-deoxycytidine (5-aza-dC), a DNA methyltransferase inhiBitor, the long-term LDR-induced gloBal genomic DNA hypermethylation was decreased and the AR was eliminated. GloBal genomic DNA hypermethylation accompanied with increases of DNMT1 and MeCP2 expression and heterochromatin formation might Be involved in long-term LDR-induced adaptive response.
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effects of long term low dose γ rays exposure on radiosensitivity of human B lymphoBlast cells
Chinese journal of radiological medicine and protection, 2013Co-Authors: Y E Shuang, Dexiao Yuan, Yuexia Xie, Yan Pan, Chunlin ShaoAbstract:OBjective To investigate the effects of long-term low-dose radiation (LDR) of γ-rays on the proliferation and radiosensitivity of human lymphoBlast cells HMy2.CIR (HMy) and to elucidate the underlying mechanism.Methods HMy cells were divided into control group and long-term LDR group.For the long-term LDR treatment,HMy cells were fractionally exposed to a low dose of γ-rays,which could enhance cell proliferation,3 times per week for 4 weeks.After the long-term LDR exposure,part of the control and long-term LDR exposed cells were further irradiated with a challenging dose (2 Gy) of γ-rays.Then cell proliferation and radiosensitivity were assayed By CCK-8 kit,cell apoptosis,and γ-H2AX formation was measured By flow cytometry.Gene expressions of cyclinD1,PCNA,Bcl-2 and Bax were detected By RT-PCR.Results The long-term LDR significantly increased cell proliferation (t =9.607,P ＜ 0.01) accompanied with up-regulation of cell cycle regulation gene cyclinD1 (t =6.869,P ＜ 0.01),proliferation regulation gene PCNA (proliferating cell nuclear antigen) (t =9.229,P ＜ 0.01) and Bcl-2 gene (t =2.662,P ＜ 0.05),But decreased the expression of pro-apoptotic gene Bax (t =19.908,P ＜0.01) in HMy cells.Compared to untreated cells,the long-term LDR decreased cell radiosensitivity (t =8.896,P ＜ 0.01),including apoptosis induction (t =4.762,P ＜ 0.01) and γ-H2AX formation (t =10.264,P＜0.01).Conclusions The long-term LDR promoted cell proliferation By up-regulating cell cycle related genes,while it reduced the radiosensitivity of HMy cells with acquisition of apoptotic resistance. Key words: Low-dose-radiation ; Cell proliferation ; Radiosensitivity ; Apoptosis ; Gene expressions
