2, 3, 7, 8-Tetrachlorodibenzo-P-Dioxin (TCDD) Induces Premature Senescence in Human and Rodent Neuronal Cells via ROS-Dependent Mechanisms
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{"title"=>"2,3,7,8-Tetrachlorodibenzo-P-Dioxin (TCDD) induces premature senescence in human and rodent neuronal cells via ROS-dependent mechanisms", "type"=>"journal", "authors"=>[{"first_name"=>"Chunhua", "last_name"=>"Wan", "scopus_author_id"=>"55682722500"}, {"first_name"=>"Jiao", "last_name"=>"Liu", "scopus_author_id"=>"55683127000"}, {"first_name"=>"Xiaoke", "last_name"=>"Nie", "scopus_author_id"=>"55701581800"}, {"first_name"=>"Jianya", "last_name"=>"Zhao", "scopus_author_id"=>"55849207800"}, {"first_name"=>"Songlin", "last_name"=>"Zhou", "scopus_author_id"=>"8218316000"}, {"first_name"=>"Zhiqing", "last_name"=>"Duan", "scopus_author_id"=>"55682840100"}, {"first_name"=>"Cuiying", "last_name"=>"Tang", "scopus_author_id"=>"56067238900"}, {"first_name"=>"Lingwei", "last_name"=>"Liang", "scopus_author_id"=>"56067201100"}, {"first_name"=>"Guangfei", "last_name"=>"Xu", "scopus_author_id"=>"55316061400"}], "year"=>2014, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-84896069552", "pmid"=>"24587053", "sgr"=>"84896069552", "doi"=>"10.1371/journal.pone.0089811", "issn"=>"19326203", "pui"=>"372599095"}, "id"=>"ae24a35f-787d-3e16-b932-6c6070384604", "abstract"=>"The widespread environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent toxicant that causes significant neurotoxicity. However, the biological events that participate in this process remain largely elusive. In the present study, we demonstrated that TCDD exposure triggered apparent premature senescence in rat pheochromocytoma (PC12) and human neuroblastoma SH-SY5Y cells. Senescence-associated ?-galactosidase (SA-?-Gal) assay revealed that TCDD induced senescence in PC12 neuronal cells at doses as low as 10 nM. TCDD led to F-actin reorganization and the appearance of an alternative senescence marker, ?-H2AX foci, both of which are important features of cellular senescence. In addition, TCDD exposure altered the expression of senescence marker proteins, such as p16, p21 and p-Rb, in both dose- and time-dependent manners. Furthermore, we demonstrated that TCDD promotes mitochondrial dysfunction and the accumulation of cellular reactive oxygen species (ROS) in PC12 cells, leading to the activation of signaling pathways that are involved in ROS metabolism and senescence. TCDD-induced ROS generation promoted significant oxidative DNA damage and lipid peroxidation. Notably, treatment with the ROS scavenger N-acetylcysteine (NAC) markedly attenuated TCDD-induced ROS production, cellular oxidative damage and neuronal senescence. Moreover, we found that TCDD induced a similar ROS-mediated senescence response in human neuroblastoma SH-SY5Y cells. In sum, these results demonstrate for the first time that TCDD induces premature senescence in neuronal cells by promoting intracellular ROS production, supporting the idea that accelerating the onset of neuronal senescence may be an important mechanism underlying TCDD-induced neurotoxic effects. ? 2014 Wan et al.", "link"=>"http://www.mendeley.com/research/2378tetrachlorodibenzopdioxin-tcdd-induces-premature-senescence-human-rodent-neuronal-cells-via-rosd", "reader_count"=>13, "reader_count_by_academic_status"=>{"Unspecified"=>1, "Researcher"=>2, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>4, "Student > Bachelor"=>3, "Professor"=>2}, "reader_count_by_user_role"=>{"Unspecified"=>1, "Researcher"=>2, "Student > Doctoral Student"=>1, "Student > Ph. D. Student"=>4, "Student > Bachelor"=>3, "Professor"=>2}, "reader_count_by_subject_area"=>{"Unspecified"=>3, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>3, "Medicine and Dentistry"=>1, "Agricultural and Biological Sciences"=>4, "Chemistry"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>1}, "Chemistry"=>{"Chemistry"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>4}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>3}, "Unspecified"=>{"Unspecified"=>3}, "Environmental Science"=>{"Environmental Science"=>1}}, "group_count"=>0}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/1396318"], "description"=>"<p>(A) SH-SY5Y cells were incubated with DMSO, 10 nM TCDD (B), 30 nM TCDD, 50 nM TCDD or 50 nM TCDD combined with 5 mM NAC. Seventy-two hours later, the cells were subjected to an SA-β-Gal assay. The percentage of β-Gal-positive cells in each group was counted and presented (* p<0.05, statistically significant difference from the control group; # p<0.05, statistically significant difference from the 50 nM TCDD-treated group). (B) TCDD exposure altered the expression of senescence marker proteins in an ROS-dependent manner in SH-SY5Y cells. SH-SY5Y cells were exposed to DMSO, 50 nM TCDD or 50 nM TCDD+5 mM NAC and then subjected to western blot analyses to determine p16, p21 and p-Rb expression. (C) Quantitative analysis of the intensity of protein expression relative to GAPDH in the indicated groups (* p<0.05, statistically significant difference from the DMSO-treated group; # p<0.05, statistically significant difference from the 50 nM TCDD-treated group).</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "premature", "senescence", "neuroblastoma", "sh-sy5y"], "article_id"=>942765, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g008", "stats"=>{"downloads"=>0, "page_views"=>109, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_TCDD_induces_premature_senescence_in_the_human_neuroblastoma_SH_SY5Y_cell_line_/942765", "title"=>"TCDD induces premature senescence in the human neuroblastoma SH-SY5Y cell line.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396314"], "description"=>"<p>(A) PC12 cells were pre-treated with DMSO, 50 nM TCDD, or 50 nM TCDD plus 5 mM NAC for 72 h before SA-β-Gal staining was performed. (B) The number of positive cells out of every 500 cells was counted and presented (* and # p<0.05, statistically significant difference from the control group; # p<0.05, statistically significant difference from the TCDD-treated group). (C) Western blot analysis of the senescence marker proteins, p16 and p21, after the cells had been treated with DMSO, 50 nM TCDD, or 50 nM TCDD and NAC for 72 h. (D) Statistical analysis of the densitometric evaluation of the three independent experiments (* p<0.05, statistically significant difference from the control group; # p<0.05, statistically significant difference from the TCDD-treated group).</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "inhibited", "tcdd-induced", "senescence", "pc12", "neuronal"], "article_id"=>942761, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g007", "stats"=>{"downloads"=>4, "page_views"=>130, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_NAC_inhibited_TCDD_induced_senescence_in_PC12_neuronal_cells_/942761", "title"=>"NAC inhibited TCDD-induced senescence in PC12 neuronal cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396312"], "description"=>"<p>(A) PC12 cells were treated with DMSO or 50 nM TCDD for 72 h. The cells were then stained to examine ROS fluorescence and visualized under a fluorescence microscope. Rosup (10 µmol/L) was used as a positive control. (B) The level of ROS fluorescence in each group was determined using a flow cytometric analysis (* p<0.05, statistically significant difference from the control group). (C) PC12 cells treated with DMSO or 50 nM TCDD for 48 h were analyzed for relative mitochondrial membrane potential using JC-1 fluorescence (* p<0.05, statistically significant difference from the control group). (D) Determination of mitochondrial H<sub>2</sub>O<sub>2</sub> production in DMSO or 50 nM TCDD-treated PC12 cells using western blot analysis. The mitochondria were prepared from DMSO- or 50 nM TCDD-treated PC12 cells and assayed for H<sub>2</sub>O<sub>2</sub> production using succinate as a substrate (* p<0.05, statistically significant difference from the control group).</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "ros", "accumulation", "dna", "pc12"], "article_id"=>942759, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g005", "stats"=>{"downloads"=>4, "page_views"=>21, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_TCDD_induces_ROS_accumulation_and_DNA_damage_in_PC12_cells_/942759", "title"=>"TCDD induces ROS accumulation and DNA damage in PC12 cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396313"], "description"=>"<p>(A) ROS fluorescence was examined in PC12 cells that had been treated with DMSO, 50 nM TCDD or 50 nM TCDD plus NAC. (B) Flow cytometric analysis of ROS fluorescence in each group. (C) PC12 cells treated with DMSO, 50 nM TCDD or 50 nM TCDD plus NAC for 72 h were immunostained with an anti-8-oxo-dG antibody. (D) Determination of lipid oxidation by analyzing the MDA content per milligram of total protein of PC12 cells after DMSO, 50 nM TCDD or 50 nM TCDD plus NAC treatment for 72 h (* p<0.05, statistically significant difference from the control group; # p<0.05, statistically significant difference from the TCDD-treated group).</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "oxidative", "dna", "lipid", "attenuated", "ros", "scavenger"], "article_id"=>942760, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g006", "stats"=>{"downloads"=>2, "page_views"=>16, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_TCDD_induced_oxidative_DNA_and_lipid_damage_were_attenuated_by_the_ROS_scavenger_NAC_/942760", "title"=>"TCDD-induced oxidative DNA and lipid damage were attenuated by the ROS scavenger NAC.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396311"], "description"=>"<p>PC12 cells were treated with DMSO, 50-transcribed into cDNA. The cDNAs were subjected to real time PCR analyses to detect the relative expression levels of the indicated genes.</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "mrna", "phenotype-related", "genes", "tcdd"], "article_id"=>942758, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g004", "stats"=>{"downloads"=>1, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Determination_of_the_mRNA_expression_levels_of_phenotype_related_genes_after_TCDD_exposure_/942758", "title"=>"Determination of the mRNA expression levels of phenotype-related genes after TCDD exposure.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396307"], "description"=>"<p>(A) Upper panel: PC12 cells were treated with DMSO or 1, 10, 50 and 100 nM TCDD for 72 h and then subjected to an SA-β-Gal staining assay. Lower panel: PC12 cells were treated with 50 nM TCDD for 0, 24, 48, 72 and 96 h and then subjected to an SA-β-Gal staining assay. (B) The number of SA-β-Gal positive cells in each group from Fig. 1A was counted and listed (* p<0.05, significantly different from the DMSO-treated group). (C) PC12 cells were treated with DMSO or 50 nM TCDD for 72 h and then immunostained with FITC–phalloidin to visualize F-actin. (D) PC12 cells were treated with DMSO or 50 nM TCDD for 72 h and were immunostained with a γ-H2AX antibody.</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "premature", "senescence", "pc12", "neuronal"], "article_id"=>942754, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g001", "stats"=>{"downloads"=>2, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_TCDD_induces_premature_senescence_in_PC12_neuronal_cells_/942754", "title"=>"TCDD induces premature senescence in PC12 neuronal cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396319", "https://ndownloader.figshare.com/files/1396320"], "description"=>"<div><p>The widespread environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent toxicant that causes significant neurotoxicity. However, the biological events that participate in this process remain largely elusive. In the present study, we demonstrated that TCDD exposure triggered apparent premature senescence in rat pheochromocytoma (PC12) and human neuroblastoma SH-SY5Y cells. Senescence-associated β-galactosidase (SA-β-Gal) assay revealed that TCDD induced senescence in PC12 neuronal cells at doses as low as 10 nM. TCDD led to F-actin reorganization and the appearance of an alternative senescence marker, γ-H2AX foci, both of which are important features of cellular senescence. In addition, TCDD exposure altered the expression of senescence marker proteins, such as p16, p21 and p-Rb, in both dose- and time-dependent manners. Furthermore, we demonstrated that TCDD promotes mitochondrial dysfunction and the accumulation of cellular reactive oxygen species (ROS) in PC12 cells, leading to the activation of signaling pathways that are involved in ROS metabolism and senescence. TCDD-induced ROS generation promoted significant oxidative DNA damage and lipid peroxidation. Notably, treatment with the ROS scavenger N-acetylcysteine (NAC) markedly attenuated TCDD-induced ROS production, cellular oxidative damage and neuronal senescence. Moreover, we found that TCDD induced a similar ROS-mediated senescence response in human neuroblastoma SH-SY5Y cells. In sum, these results demonstrate for the first time that TCDD induces premature senescence in neuronal cells by promoting intracellular ROS production, supporting the idea that accelerating the onset of neuronal senescence may be an important mechanism underlying TCDD-induced neurotoxic effects.</p></div>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "8-tetrachlorodibenzo-p-dioxin", "premature", "senescence", "rodent", "neuronal", "cells", "ros-dependent"], "article_id"=>942766, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0089811.s001", "https://dx.doi.org/10.1371/journal.pone.0089811.s002"], "stats"=>{"downloads"=>3, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_2_3_7_8_Tetrachlorodibenzo_P_Dioxin_TCDD_Induces_Premature_Senescence_in_Human_and_Rodent_Neuronal_Cells_via_ROS_Dependent_Mechanisms_/942766", "title"=>"2, 3, 7, 8-Tetrachlorodibenzo-P-Dioxin (TCDD) Induces Premature Senescence in Human and Rodent Neuronal Cells via ROS-Dependent Mechanisms", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396310"], "description"=>"<p>(A) PC12 cells were exposed to 50 nM TCDD for 24, 48, 72 or 96 h and then harvested for western blot analyses using anti-p16, anti-p21 and anti-p-Rb antibodies. T, TCDD-treated cells; C, control group. (B) Quantitative analysis of the intensity of protein expression relative to GAPDH in the indicated groups (*, # and ∧ p<0.05, statistically significant difference from the control group).</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "senescence", "tcdd"], "article_id"=>942757, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g003", "stats"=>{"downloads"=>1, "page_views"=>3, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Time_dependency_of_senescence_marker_protein_expression_after_TCDD_exposure_/942757", "title"=>"Time-dependency of senescence marker protein expression after TCDD exposure.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/1396309"], "description"=>"<p>PC12 cells were exposed to different doses of TCDD for 72(A) and semi-quantitative PCR (B) analyses to determine the protein and mRNA levels of p16 (* p<0.05, significantly different from the DMSO-treated group). (C) The expression of p21 and p-Rb was also evaluated using a western blot analysis (* p<0.05, significantly different from the DMSO-treated group).</p>", "links"=>[], "tags"=>["Molecular cell biology", "Cellular types", "neurons", "Cell death", "cell division", "Cellular stress responses", "gene expression", "toxicology", "Neurotoxicology", "Public health", "Environmental health", "Toxic agents", "induced", "senescence", "proteins", "dose-dependent"], "article_id"=>942756, "categories"=>["Biological Sciences", "Medicine"], "users"=>["Chunhua Wan", "Jiao Liu", "Xiaoke Nie", "Jianya Zhao", "Songlin Zhou", "Zhiqing Duan", "Cuiying Tang", "Lingwei Liang", "Guangfei Xu"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0089811.g002", "stats"=>{"downloads"=>2, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_TCDD_induced_the_expression_of_senescence_marker_proteins_in_a_dose_dependent_manner_/942756", "title"=>"TCDD induced the expression of senescence marker proteins in a dose-dependent manner.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2014-02-24 02:59:13"}

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