Arsenic induces human chondrocyte senescence and accelerates rat articular cartilage aging
Arsenic-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 bo...
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| Veröffentlicht in: | Archives of toxicology 2020, Vol.94 (1), p.89-101 |
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| creator | Chung, Yao-Pang Chen, Ya-Wen Weng, Te-I Yang, Rong-Sen Liu, Shing-Hwa |
| description | Arsenic-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 (As
2
O
3
; 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. |
| doi_str_mv | 10.1007/s00204-019-02607-2 |
| format | Article |
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2
O
3
; 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.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s00204-019-02607-2</identifier><identifier>PMID: 31734849</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Abrasion ; Aging ; Animals ; Arsenic ; Arsenic - toxicity ; Arsenic trioxide ; Arthritis ; Biomedical and Life Sciences ; Biomedical materials ; Biomedicine ; c-Jun protein ; Cartilage ; Cartilage (articular) ; Cartilage, Articular - drug effects ; Cartilage, Articular - metabolism ; Cartilage, Articular - physiopathology ; Cells, Cultured ; Cellular Senescence - drug effects ; Chondrocytes ; Chondrocytes - cytology ; Chondrocytes - drug effects ; Chondrogenesis ; Collagenase 3 ; Differentiation (biology) ; Drinking water ; Environmental Health ; Epidemiology ; Exposure ; Galactosidase ; GATA4 Transcription Factor - metabolism ; Gene expression ; GTP-binding protein ; Humans ; Inorganic Compounds ; JNK protein ; Kinases ; Male ; MAP Kinase Signaling System - drug effects ; Mesenchyme ; Monocyte chemoattractant protein 1 ; NF-kappa B - metabolism ; NF-κB protein ; Occupational Medicine/Industrial Medicine ; p38 Mitogen-Activated Protein Kinases - metabolism ; p53 Protein ; Pharmacology/Toxicology ; Phenotypes ; Phosphorylation ; Proteins ; Rats, Wistar ; Senescence ; Signaling ; Stem cells ; Toxicity Tests ; Transcription factors ; Water pollution ; β-Galactosidase</subject><ispartof>Archives of toxicology, 2020, Vol.94 (1), p.89-101</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2019</rights><rights>Archives of Toxicology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-bddd113e925887591e51c2f68858e77256d354b0e01ab222fb5ff6e5eecf358b3</citedby><cites>FETCH-LOGICAL-c375t-bddd113e925887591e51c2f68858e77256d354b0e01ab222fb5ff6e5eecf358b3</cites><orcidid>0000-0002-9976-1197</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00204-019-02607-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00204-019-02607-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31734849$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chung, Yao-Pang</creatorcontrib><creatorcontrib>Chen, Ya-Wen</creatorcontrib><creatorcontrib>Weng, Te-I</creatorcontrib><creatorcontrib>Yang, Rong-Sen</creatorcontrib><creatorcontrib>Liu, Shing-Hwa</creatorcontrib><title>Arsenic induces human chondrocyte senescence and accelerates rat articular cartilage aging</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><addtitle>Arch Toxicol</addtitle><description>Arsenic-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 (As
2
O
3
; 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.</description><subject>Abrasion</subject><subject>Aging</subject><subject>Animals</subject><subject>Arsenic</subject><subject>Arsenic - toxicity</subject><subject>Arsenic trioxide</subject><subject>Arthritis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedical materials</subject><subject>Biomedicine</subject><subject>c-Jun protein</subject><subject>Cartilage</subject><subject>Cartilage (articular)</subject><subject>Cartilage, Articular - drug effects</subject><subject>Cartilage, Articular - metabolism</subject><subject>Cartilage, Articular - physiopathology</subject><subject>Cells, Cultured</subject><subject>Cellular Senescence - drug effects</subject><subject>Chondrocytes</subject><subject>Chondrocytes - cytology</subject><subject>Chondrocytes - drug effects</subject><subject>Chondrogenesis</subject><subject>Collagenase 3</subject><subject>Differentiation (biology)</subject><subject>Drinking water</subject><subject>Environmental Health</subject><subject>Epidemiology</subject><subject>Exposure</subject><subject>Galactosidase</subject><subject>GATA4 Transcription Factor - metabolism</subject><subject>Gene expression</subject><subject>GTP-binding protein</subject><subject>Humans</subject><subject>Inorganic Compounds</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Male</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Mesenchyme</subject><subject>Monocyte chemoattractant protein 1</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Occupational Medicine/Industrial Medicine</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>p53 Protein</subject><subject>Pharmacology/Toxicology</subject><subject>Phenotypes</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Rats, Wistar</subject><subject>Senescence</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Toxicity Tests</subject><subject>Transcription factors</subject><subject>Water pollution</subject><subject>β-Galactosidase</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kD1PwzAQhi0EoiXwBxhQJObA2Y5jZ6wqvqRKLLCwRI5zSVOlTrGTof8elxTYkCz7pHvuPfkh5JrCHQWQ9x6AQZoAzRNgGciEnZA5TTlLQHJ1SubAU0iEzOiMXHi_AaBM5fyczDiVPFVpPicfC-fRtiZubTUa9PF63Gobm3VvK9eb_YBx6KM3aA3G2laxNgY7dHoIcLhj7YbWjJ12sTmUnW4C17S2uSRnte48Xh3fiLw_Prwtn5PV69PLcrFKDJdiSMqqqijlmDOhlBQ5RUENqzOlhEIpmcgqLtISEKguGWN1Keo6Q4Foai5UySNyO-XuXP85oh-KTT86G1YWLPwy44qHExE2Ucb13jusi51rt9rtCwrFQWcx6SyCzuJbZ5iOyM0xeiy3WP2O_PgLAJ8AH1q2Qfe3-5_YL8DJgK4</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Chung, Yao-Pang</creator><creator>Chen, Ya-Wen</creator><creator>Weng, Te-I</creator><creator>Yang, Rong-Sen</creator><creator>Liu, Shing-Hwa</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T2</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0002-9976-1197</orcidid></search><sort><creationdate>2020</creationdate><title>Arsenic induces human chondrocyte senescence and accelerates rat articular cartilage aging</title><author>Chung, Yao-Pang ; Chen, Ya-Wen ; Weng, Te-I ; Yang, Rong-Sen ; Liu, Shing-Hwa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-bddd113e925887591e51c2f68858e77256d354b0e01ab222fb5ff6e5eecf358b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Abrasion</topic><topic>Aging</topic><topic>Animals</topic><topic>Arsenic</topic><topic>Arsenic - toxicity</topic><topic>Arsenic trioxide</topic><topic>Arthritis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedical materials</topic><topic>Biomedicine</topic><topic>c-Jun protein</topic><topic>Cartilage</topic><topic>Cartilage (articular)</topic><topic>Cartilage, Articular - drug effects</topic><topic>Cartilage, Articular - metabolism</topic><topic>Cartilage, Articular - physiopathology</topic><topic>Cells, Cultured</topic><topic>Cellular Senescence - drug effects</topic><topic>Chondrocytes</topic><topic>Chondrocytes - cytology</topic><topic>Chondrocytes - drug effects</topic><topic>Chondrogenesis</topic><topic>Collagenase 3</topic><topic>Differentiation (biology)</topic><topic>Drinking water</topic><topic>Environmental Health</topic><topic>Epidemiology</topic><topic>Exposure</topic><topic>Galactosidase</topic><topic>GATA4 Transcription Factor - metabolism</topic><topic>Gene expression</topic><topic>GTP-binding protein</topic><topic>Humans</topic><topic>Inorganic Compounds</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Male</topic><topic>MAP Kinase Signaling System - 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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 (As
2
O
3
; 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.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31734849</pmid><doi>10.1007/s00204-019-02607-2</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-9976-1197</orcidid></addata></record> |
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| ispartof | Archives of toxicology, 2020, Vol.94 (1), p.89-101 |
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| subjects | Abrasion Aging Animals Arsenic Arsenic - toxicity Arsenic trioxide Arthritis Biomedical and Life Sciences Biomedical materials Biomedicine c-Jun protein Cartilage Cartilage (articular) Cartilage, Articular - drug effects Cartilage, Articular - metabolism Cartilage, Articular - physiopathology Cells, Cultured Cellular Senescence - drug effects Chondrocytes Chondrocytes - cytology Chondrocytes - drug effects Chondrogenesis Collagenase 3 Differentiation (biology) Drinking water Environmental Health Epidemiology Exposure Galactosidase GATA4 Transcription Factor - metabolism Gene expression GTP-binding protein Humans Inorganic Compounds JNK protein Kinases Male MAP Kinase Signaling System - drug effects Mesenchyme Monocyte chemoattractant protein 1 NF-kappa B - metabolism NF-κB protein Occupational Medicine/Industrial Medicine p38 Mitogen-Activated Protein Kinases - metabolism p53 Protein Pharmacology/Toxicology Phenotypes Phosphorylation Proteins Rats, Wistar Senescence Signaling Stem cells Toxicity Tests Transcription factors Water pollution β-Galactosidase |
| title | Arsenic induces human chondrocyte senescence and accelerates rat articular cartilage aging |
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