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  1. NTU Scholars
  2. 醫學院
  3. 法醫學科所
Please use this identifier to cite or link to this item: https://scholars.lib.ntu.edu.tw/handle/123456789/508534
DC FieldValueLanguage
dc.contributor.authorChung Y.-P.en_US
dc.contributor.authorChen Y.-W.en_US
dc.contributor.authorTE-I WENGen_US
dc.contributor.authorRONG-SEN YANGen_US
dc.contributor.authorSHING-HWA LIUen_US
dc.creatorChung Y.-P.;Chen Y.-W.;Te-I Weng;Yang R.-S.;Liu S.-H.-
dc.date.accessioned2020-07-05T01:53:58Z-
dc.date.available2020-07-05T01:53:58Z-
dc.date.issued2020-
dc.identifier.issn0340-5761-
dc.identifier.urihttps://scholars.lib.ntu.edu.tw/handle/123456789/508534-
dc.description.abstractArsenic-contaminated drinking water is known to be a serious human health problem. A previous epidemiological study has indicated that arsenic levels in blood were higher in arthritis patients compared to age-matched control subjects. Bone is known as an important arsenic store compartment in the body. Arsenic exposure has been suggested to promote senescence in human mesenchymal stem cells that may affect the balance of adipogenic and osteogenic differentiation. The toxicological effect and mechanism of arsenic exposure on articular chondrocytes still remain unclear. Here, we investigated the arsenic-induced senescence in cultured human articular chondrocytes and long-term arsenic-exposed rat articular cartilage. Arsenic trioxide (As2O3; 1–5?μM) significantly induced senescence in human articular chondrocytes by increasing senescence-associated β-galactosidase (SA-β-Gal) activity and protein expression of p16, p53, and p21. Arsenic induced the phosphorylation of p38 and c-Jun N-terminal kinase (JNK) proteins. The inhibitors of p38 and JNK significantly reversed the arsenic-induced chondrocyte senescence. Arsenic could also trigger the induction of GATA4-NF-κB signaling and senescence-associated secretory phenotype (SASP) by increasing IL-1α, IL-1β, TGF-β, TNF-α, CCL2, PAI-1, and MMP13 mRNA expression. The increased cartilage senescence and abrasion were also observed in a rat model long-term treatment with arsenic (0.05 and 0.5?ppm) in drinking water for 36?weeks as compared to age-matched control rats. The phosphorylation of p38 and JNK and the induction of GATA4-NF-κB signaling and SASP were enhanced in the rat cartilages. Taken together, these findings suggest that arsenic exposure is capable of inducing chondrocyte senescence and accelerating rat articular cartilage aging and abrasion. ? 2019, Springer-Verlag GmbH Germany, part of Springer Nature.-
dc.relation.ispartofArchives of Toxicology-
dc.subject.otherarsenic; arsenic trioxide; beta galactosidase; collagenase 3; drinking water; immunoglobulin enhancer binding protein; interleukin 1alpha; interleukin 1beta; messenger RNA; protein p16; protein p21; protein p53; stress activated protein kinase; synaptophysin; transcription factor GATA 4; transforming growth factor beta; tumor necrosis factor; arsenic; GATA4 protein, human; immunoglobulin enhancer binding protein; mitogen activated protein kinase p38; transcription factor GATA 4; animal cell; animal experiment; animal model; Article; articular cartilage; cell aging; chondrocyte; controlled study; flow cytometry; human; human cell; human tissue; male; nonhuman; priority journal; protein expression; rat; signal transduction; animal; articular cartilage; cell aging; cell culture; chondrocyte; cytology; drug effect; MAPK signaling; metabolism; pathophysiology; toxicity testing; Wistar rat; Animals; Arsenic; Cartilage, Articular; Cells, Cultured; Cellular Senescence; Chondrocytes; GATA4 Transcription Factor; Humans; Male; MAP Kinase Signaling System; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Rats, Wistar; Toxicity Tests-
dc.subject.other[SDGs]SDG3-
dc.titleArsenic induces human chondrocyte senescence and accelerates rat articular cartilage agingen_US
dc.typeJournal Article-
dc.identifier.doi10.1007/s00204-019-02607-2-
dc.identifier.pmid31734849-
dc.identifier.scopus2-s2.0-85075361663-
dc.relation.pages89-101-
dc.relation.journalvolume94-
dc.relation.journalissue1-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.fulltextno fulltext-
item.cerifentitytypePublications-
crisitem.author.deptForensic Medicine-
crisitem.author.deptEmergency Medicine-NTUH-
crisitem.author.deptOrthopedic Surgery-NTUH-
crisitem.author.deptOrthopedic Surgery-
crisitem.author.deptToxicology-
crisitem.author.orcid0000-0002-8797-1672-
crisitem.author.orcid0000-0002-0553-4779-
crisitem.author.orcid0000-0002-9976-1197-
crisitem.author.parentorgCollege of Medicine-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgNational Taiwan University Hospital-
crisitem.author.parentorgCollege of Medicine-
crisitem.author.parentorgCollege of Medicine-
Appears in Collections:法醫學科所
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臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of “NTU Repository” with “Academic Hub” to form NTU Scholars.

總館學科館員 (Main Library)
醫學圖書館學科館員 (Medical Library)
社會科學院辜振甫紀念圖書館學科館員 (Social Sciences Library)

開放取用是從使用者角度提升資訊取用性的社會運動,應用在學術研究上是透過將研究著作公開供使用者自由取閱,以促進學術傳播及因應期刊訂購費用逐年攀升。同時可加速研究發展、提升研究影響力,NTU Scholars即為本校的開放取用典藏(OA Archive)平台。(點選深入了解OA)

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