lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1
Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RN...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
FangPing Liao [verfasserIn] Yi Tan [verfasserIn] YuYu Wang [verfasserIn] CaiLan Zhou [verfasserIn] QiuLing Wang [verfasserIn] JingLin Li [verfasserIn] LiMei He [verfasserIn] XiaoWu Peng [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Ecotoxicology and Environmental Safety - Elsevier, 2021, 226(2021), Seite 112834- |
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| Übergeordnetes Werk: |
volume:226 ; year:2021 ; pages:112834- |
| Links: |
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| DOI / URN: |
10.1016/j.ecoenv.2021.112834 |
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| Katalog-ID: |
DOAJ077105850 |
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| 245 | 1 | 0 | |a lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 |
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| 520 | |a Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. | ||
| 650 | 4 | |a PM2.5 | |
| 650 | 4 | |a lncRNA AABR07005593.1 | |
| 650 | 4 | |a Respiratory inflammation | |
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| 700 | 0 | |a QiuLing Wang |e verfasserin |4 aut | |
| 700 | 0 | |a JingLin Li |e verfasserin |4 aut | |
| 700 | 0 | |a LiMei He |e verfasserin |4 aut | |
| 700 | 0 | |a XiaoWu Peng |e verfasserin |4 aut | |
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10.1016/j.ecoenv.2021.112834 doi (DE-627)DOAJ077105850 (DE-599)DOAJ9c8f05b4575a4aac934566ece09e94a3 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 FangPing Liao verfasserin aut lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. PM2.5 lncRNA AABR07005593.1 Respiratory inflammation Environmental pollution Environmental sciences Yi Tan verfasserin aut YuYu Wang verfasserin aut CaiLan Zhou verfasserin aut QiuLing Wang verfasserin aut JingLin Li verfasserin aut LiMei He verfasserin aut XiaoWu Peng verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 226(2021), Seite 112834- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:226 year:2021 pages:112834- https://doi.org/10.1016/j.ecoenv.2021.112834 kostenfrei https://doaj.org/article/9c8f05b4575a4aac934566ece09e94a3 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321009465 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 226 2021 112834- |
| spelling |
10.1016/j.ecoenv.2021.112834 doi (DE-627)DOAJ077105850 (DE-599)DOAJ9c8f05b4575a4aac934566ece09e94a3 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 FangPing Liao verfasserin aut lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. PM2.5 lncRNA AABR07005593.1 Respiratory inflammation Environmental pollution Environmental sciences Yi Tan verfasserin aut YuYu Wang verfasserin aut CaiLan Zhou verfasserin aut QiuLing Wang verfasserin aut JingLin Li verfasserin aut LiMei He verfasserin aut XiaoWu Peng verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 226(2021), Seite 112834- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:226 year:2021 pages:112834- https://doi.org/10.1016/j.ecoenv.2021.112834 kostenfrei https://doaj.org/article/9c8f05b4575a4aac934566ece09e94a3 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321009465 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 226 2021 112834- |
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10.1016/j.ecoenv.2021.112834 doi (DE-627)DOAJ077105850 (DE-599)DOAJ9c8f05b4575a4aac934566ece09e94a3 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 FangPing Liao verfasserin aut lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. PM2.5 lncRNA AABR07005593.1 Respiratory inflammation Environmental pollution Environmental sciences Yi Tan verfasserin aut YuYu Wang verfasserin aut CaiLan Zhou verfasserin aut QiuLing Wang verfasserin aut JingLin Li verfasserin aut LiMei He verfasserin aut XiaoWu Peng verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 226(2021), Seite 112834- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:226 year:2021 pages:112834- https://doi.org/10.1016/j.ecoenv.2021.112834 kostenfrei https://doaj.org/article/9c8f05b4575a4aac934566ece09e94a3 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321009465 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 226 2021 112834- |
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10.1016/j.ecoenv.2021.112834 doi (DE-627)DOAJ077105850 (DE-599)DOAJ9c8f05b4575a4aac934566ece09e94a3 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 FangPing Liao verfasserin aut lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. PM2.5 lncRNA AABR07005593.1 Respiratory inflammation Environmental pollution Environmental sciences Yi Tan verfasserin aut YuYu Wang verfasserin aut CaiLan Zhou verfasserin aut QiuLing Wang verfasserin aut JingLin Li verfasserin aut LiMei He verfasserin aut XiaoWu Peng verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 226(2021), Seite 112834- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:226 year:2021 pages:112834- https://doi.org/10.1016/j.ecoenv.2021.112834 kostenfrei https://doaj.org/article/9c8f05b4575a4aac934566ece09e94a3 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321009465 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 226 2021 112834- |
| allfieldsSound |
10.1016/j.ecoenv.2021.112834 doi (DE-627)DOAJ077105850 (DE-599)DOAJ9c8f05b4575a4aac934566ece09e94a3 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 FangPing Liao verfasserin aut lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. PM2.5 lncRNA AABR07005593.1 Respiratory inflammation Environmental pollution Environmental sciences Yi Tan verfasserin aut YuYu Wang verfasserin aut CaiLan Zhou verfasserin aut QiuLing Wang verfasserin aut JingLin Li verfasserin aut LiMei He verfasserin aut XiaoWu Peng verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 226(2021), Seite 112834- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:226 year:2021 pages:112834- https://doi.org/10.1016/j.ecoenv.2021.112834 kostenfrei https://doaj.org/article/9c8f05b4575a4aac934566ece09e94a3 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321009465 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 226 2021 112834- |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ077105850</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230309150456.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230228s2021 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.ecoenv.2021.112834</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ077105850</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ9c8f05b4575a4aac934566ece09e94a3</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">TD172-193.5</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">GE1-350</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">FangPing Liao</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. 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TD172-193.5 GE1-350 lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 PM2.5 lncRNA AABR07005593.1 Respiratory inflammation |
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lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 |
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lncrna aabr07005593.1 potentiates pm2.5-induced interleukin-6 expression by targeting mccc1 |
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lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 |
| abstract |
Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. |
| abstractGer |
Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. |
| abstract_unstemmed |
Background: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. Objective: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. Methods: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 μM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. Results: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. Conclusion: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation. |
| collection_details |
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| title_short |
lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1 |
| url |
https://doi.org/10.1016/j.ecoenv.2021.112834 https://doaj.org/article/9c8f05b4575a4aac934566ece09e94a3 http://www.sciencedirect.com/science/article/pii/S0147651321009465 https://doaj.org/toc/0147-6513 |
| remote_bool |
true |
| author2 |
Yi Tan YuYu Wang CaiLan Zhou QiuLing Wang JingLin Li LiMei He XiaoWu Peng |
| author2Str |
Yi Tan YuYu Wang CaiLan Zhou QiuLing Wang JingLin Li LiMei He XiaoWu Peng |
| ppnlink |
266018467 |
| callnumber-subject |
TD - Environmental Technology |
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c |
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true |
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false |
| doi_str |
10.1016/j.ecoenv.2021.112834 |
| callnumber-a |
TD172-193.5 |
| up_date |
2024-07-03T23:55:20.730Z |
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1803604114260623360 |
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| score |
7.399908 |