Possible role of PAPR-1 in protecting human HaCaT cells against cytotoxicity of SiO 2 nanoparticles
Nano-SiO materials play a significant role in the engineered nanomaterials (ENMs) field. The ease of their production as well as their relatively low cost has promoted the wide use of these products in many fields. Nano-SiO exposure is known to cause severe DNA damage; however, the underlying mechan...
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| Veröffentlicht in: | Toxicology letters 2017-10, Vol.280, p.213 |
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| creator | Gong, Chunmei Yang, Linqing Zhou, Jichang Guo, Xiang Zhuang, Zhixiong |
| description | Nano-SiO
materials play a significant role in the engineered nanomaterials (ENMs) field. The ease of their production as well as their relatively low cost has promoted the wide use of these products in many fields. Nano-SiO
exposure is known to cause severe DNA damage; however, the underlying mechanisms remain poorly understood. In a previous study, we found that nano-SiO
exposure regulate the expression of the poly(ADP-ribose) polymerases-1 (PARP-1), a pivotal DNA repair gene, in human HaCaT cells. Here, we employed lentivirus-mediated RNA interference (RNAi) to knock down PAPR-1 expression in HaCaT cells and explored the potential role of PARP-1 in nano-SiO
induced cytotoxicity. We found that nano-SiO
treatment of HaCaT cells causes decreased cell viability, increased apoptosis and DNA damage. Nano-SiO
-treated HaCaT cells were also found to have slightly changed cell cycle distribution. Lentivirus-mediated PAPR-1 knockdown partially aggravated cytotoxicity and increased apoptosis induced by nano-SiO
treatment. Nano-SiO
had significant toxicity to human HaCaT cells and causes DNA damage. PAPR-1 knock-down cell line appears more sensitive to nano-SiO
than the control cells in DNA damage. The results suggest that PAPR-1 is involved in protecting cells from damage caused by nano-SiO
. |
| doi_str_mv | 10.1016/j.toxlet.2017.07.213 |
| format | Article |
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materials play a significant role in the engineered nanomaterials (ENMs) field. The ease of their production as well as their relatively low cost has promoted the wide use of these products in many fields. Nano-SiO
exposure is known to cause severe DNA damage; however, the underlying mechanisms remain poorly understood. In a previous study, we found that nano-SiO
exposure regulate the expression of the poly(ADP-ribose) polymerases-1 (PARP-1), a pivotal DNA repair gene, in human HaCaT cells. Here, we employed lentivirus-mediated RNA interference (RNAi) to knock down PAPR-1 expression in HaCaT cells and explored the potential role of PARP-1 in nano-SiO
induced cytotoxicity. We found that nano-SiO
treatment of HaCaT cells causes decreased cell viability, increased apoptosis and DNA damage. Nano-SiO
-treated HaCaT cells were also found to have slightly changed cell cycle distribution. Lentivirus-mediated PAPR-1 knockdown partially aggravated cytotoxicity and increased apoptosis induced by nano-SiO
treatment. Nano-SiO
had significant toxicity to human HaCaT cells and causes DNA damage. PAPR-1 knock-down cell line appears more sensitive to nano-SiO
than the control cells in DNA damage. The results suggest that PAPR-1 is involved in protecting cells from damage caused by nano-SiO
.</description><identifier>EISSN: 1879-3169</identifier><identifier>DOI: 10.1016/j.toxlet.2017.07.213</identifier><identifier>PMID: 28757444</identifier><language>eng</language><publisher>Netherlands</publisher><subject>Cell Cycle - drug effects ; Cell Line ; Cell Proliferation - drug effects ; Cell Survival ; Chromosome Aberrations - chemically induced ; Gene Deletion ; Humans ; Nanoparticles - chemistry ; Nanoparticles - toxicity ; Poly (ADP-Ribose) Polymerase-1 - genetics ; Poly (ADP-Ribose) Polymerase-1 - metabolism ; Silicon Dioxide - chemistry ; Silicon Dioxide - toxicity</subject><ispartof>Toxicology letters, 2017-10, Vol.280, p.213</ispartof><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27913,27914</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28757444$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gong, Chunmei</creatorcontrib><creatorcontrib>Yang, Linqing</creatorcontrib><creatorcontrib>Zhou, Jichang</creatorcontrib><creatorcontrib>Guo, Xiang</creatorcontrib><creatorcontrib>Zhuang, Zhixiong</creatorcontrib><title>Possible role of PAPR-1 in protecting human HaCaT cells against cytotoxicity of SiO 2 nanoparticles</title><title>Toxicology letters</title><addtitle>Toxicol Lett</addtitle><description>Nano-SiO
materials play a significant role in the engineered nanomaterials (ENMs) field. The ease of their production as well as their relatively low cost has promoted the wide use of these products in many fields. Nano-SiO
exposure is known to cause severe DNA damage; however, the underlying mechanisms remain poorly understood. In a previous study, we found that nano-SiO
exposure regulate the expression of the poly(ADP-ribose) polymerases-1 (PARP-1), a pivotal DNA repair gene, in human HaCaT cells. Here, we employed lentivirus-mediated RNA interference (RNAi) to knock down PAPR-1 expression in HaCaT cells and explored the potential role of PARP-1 in nano-SiO
induced cytotoxicity. We found that nano-SiO
treatment of HaCaT cells causes decreased cell viability, increased apoptosis and DNA damage. Nano-SiO
-treated HaCaT cells were also found to have slightly changed cell cycle distribution. Lentivirus-mediated PAPR-1 knockdown partially aggravated cytotoxicity and increased apoptosis induced by nano-SiO
treatment. Nano-SiO
had significant toxicity to human HaCaT cells and causes DNA damage. PAPR-1 knock-down cell line appears more sensitive to nano-SiO
than the control cells in DNA damage. The results suggest that PAPR-1 is involved in protecting cells from damage caused by nano-SiO
.</description><subject>Cell Cycle - drug effects</subject><subject>Cell Line</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival</subject><subject>Chromosome Aberrations - chemically induced</subject><subject>Gene Deletion</subject><subject>Humans</subject><subject>Nanoparticles - chemistry</subject><subject>Nanoparticles - toxicity</subject><subject>Poly (ADP-Ribose) Polymerase-1 - genetics</subject><subject>Poly (ADP-Ribose) Polymerase-1 - metabolism</subject><subject>Silicon Dioxide - chemistry</subject><subject>Silicon Dioxide - toxicity</subject><issn>1879-3169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjs1qAjEUhUNB_H-DUu4LTJrMjBNdFmlx10FnL9cY9UomGZIInbevhbp2c87mO3yHsVcpuBSyer_y5H-sSTwXUnGheC6LFzaWS7XKClmtRmwS41UIUZXVYshG-VItVFmWY6ZrHyMdrIHg7-FPUH_U20wCOeiCT0Yncme43Fp0sME1NqCNtRHwjORiAt0nf5eTptT_zXf0DTk4dL7DkEhbE2dscEIbzfy_p-zt67NZb7LudmjNcd8FajH0-8er4inwC_EbSY4</recordid><startdate>20171005</startdate><enddate>20171005</enddate><creator>Gong, Chunmei</creator><creator>Yang, Linqing</creator><creator>Zhou, Jichang</creator><creator>Guo, Xiang</creator><creator>Zhuang, Zhixiong</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20171005</creationdate><title>Possible role of PAPR-1 in protecting human HaCaT cells against cytotoxicity of SiO 2 nanoparticles</title><author>Gong, Chunmei ; Yang, Linqing ; Zhou, Jichang ; Guo, Xiang ; Zhuang, Zhixiong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_287574443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Cell Cycle - drug effects</topic><topic>Cell Line</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival</topic><topic>Chromosome Aberrations - chemically induced</topic><topic>Gene Deletion</topic><topic>Humans</topic><topic>Nanoparticles - chemistry</topic><topic>Nanoparticles - toxicity</topic><topic>Poly (ADP-Ribose) Polymerase-1 - genetics</topic><topic>Poly (ADP-Ribose) Polymerase-1 - metabolism</topic><topic>Silicon Dioxide - chemistry</topic><topic>Silicon Dioxide - toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gong, Chunmei</creatorcontrib><creatorcontrib>Yang, Linqing</creatorcontrib><creatorcontrib>Zhou, Jichang</creatorcontrib><creatorcontrib>Guo, Xiang</creatorcontrib><creatorcontrib>Zhuang, Zhixiong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Toxicology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gong, Chunmei</au><au>Yang, Linqing</au><au>Zhou, Jichang</au><au>Guo, Xiang</au><au>Zhuang, Zhixiong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Possible role of PAPR-1 in protecting human HaCaT cells against cytotoxicity of SiO 2 nanoparticles</atitle><jtitle>Toxicology letters</jtitle><addtitle>Toxicol Lett</addtitle><date>2017-10-05</date><risdate>2017</risdate><volume>280</volume><spage>213</spage><pages>213-</pages><eissn>1879-3169</eissn><abstract>Nano-SiO
materials play a significant role in the engineered nanomaterials (ENMs) field. The ease of their production as well as their relatively low cost has promoted the wide use of these products in many fields. Nano-SiO
exposure is known to cause severe DNA damage; however, the underlying mechanisms remain poorly understood. In a previous study, we found that nano-SiO
exposure regulate the expression of the poly(ADP-ribose) polymerases-1 (PARP-1), a pivotal DNA repair gene, in human HaCaT cells. Here, we employed lentivirus-mediated RNA interference (RNAi) to knock down PAPR-1 expression in HaCaT cells and explored the potential role of PARP-1 in nano-SiO
induced cytotoxicity. We found that nano-SiO
treatment of HaCaT cells causes decreased cell viability, increased apoptosis and DNA damage. Nano-SiO
-treated HaCaT cells were also found to have slightly changed cell cycle distribution. Lentivirus-mediated PAPR-1 knockdown partially aggravated cytotoxicity and increased apoptosis induced by nano-SiO
treatment. Nano-SiO
had significant toxicity to human HaCaT cells and causes DNA damage. PAPR-1 knock-down cell line appears more sensitive to nano-SiO
than the control cells in DNA damage. The results suggest that PAPR-1 is involved in protecting cells from damage caused by nano-SiO
.</abstract><cop>Netherlands</cop><pmid>28757444</pmid><doi>10.1016/j.toxlet.2017.07.213</doi></addata></record> |
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| identifier | EISSN: 1879-3169 |
| ispartof | Toxicology letters, 2017-10, Vol.280, p.213 |
| issn | 1879-3169 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Cell Cycle - drug effects Cell Line Cell Proliferation - drug effects Cell Survival Chromosome Aberrations - chemically induced Gene Deletion Humans Nanoparticles - chemistry Nanoparticles - toxicity Poly (ADP-Ribose) Polymerase-1 - genetics Poly (ADP-Ribose) Polymerase-1 - metabolism Silicon Dioxide - chemistry Silicon Dioxide - toxicity |
| title | Possible role of PAPR-1 in protecting human HaCaT cells against cytotoxicity of SiO 2 nanoparticles |
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