Coculture SAEC and HMVEC exposed to MWCNT
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ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens
PROVIDER: GSE131121 | GEO | 2022/04/18
REPOSITORIES: GEO
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Project description:Multi-walled carbon nanotubes (MWCNT) present a wide variety of exciting application opportunities. As MWCNT are produced in large quantities, occupational exposure and human health is of particular concern. However, there is no consensus regarding their potential harmful effects. In particular, chronic exposure to MWCNT and mechanisms of their action at protein and lipid levels are unknown. In this study, we aimed to investigate effects of long-term chronic exposure to MWCNT on cellular proteome and lipidome. Since the lung is the major target organ, an in vitro normal bronchial epithelial cell model was used. To better mimic exposure at occupational settings, cells were chronically exposed for 13 weeks to low-doses of MWCNT. MWCNT-treatment increased ROS levels in cells without increasing DNA damage and resulted in differential expression of multiple apoptotic proteins. A shotgun proteomic and lipidomic analysis of the MWCNT-exposed cells showed that of amongst the >5000 identified protein s,groups; more than 200 were altered in treated cells. Functional analysis revealed association of these differentially regulated proteins in various cellular processes such as cell death and survival, cellular assembly and organization. Similarly, the lipid profile of the MWCNT treated cells showed accumulation of multiple lipid classes. This is first study to present results indicating that long-term MWCNT-exposure of human normal lung cells at occupationally relevant low-dose may alter both the proteome and the lipidome profile of target epithelial cells in the lung.
2020-05-06 | PXD005970 | Pride
Project description:Recent in vivo studies reported that inhaled carbon nanotube distribute in the alveolar region resulting in an acute inflammation, progressive fibrotic response and particle accumulation at the bronchoalveolar junction with low clearance. With similar biopersistence and shape as asbestos, a known lung carcinogen, growing concern has arisen for elevated risk of carbon nanotube-induced lung carcinogenesis; however few studies have evaluated long-term human health risks associated with chronic pulmonary carbon nanotube exposures compared to asbestos. To address this knowledge gap, we conducted subchronic in vitro exposures of dispersed single walled carbon nanotube, multi-walled carbon nanotube and crocidolite asbestos to human small airway epithelial cells to assess their neoplastic transformation potential. Subchronic single-, multi-walled carbon nanotube and asbestos exposures caused human lung cell neoplastic transformation exhibited by increased proliferation, anchorage-independent growth, invasion and angiogenesis. Whole genome profiling and protein expression analyses showed that carbon nanotube-induced transformation mechanism(s) was largely different from asbestos-related inflammatory signaling, suggesting specific carbon nanotube-induced carcinogenic potential. This study provides novel carbon nanotube and asbestos toxicogenomic information for risk assessment and an in vitro model to evaluate transformation potential of carbon nanotubes and other nanoparticles. Whole genome expression profiling was conducted on human immortalized small airway epithelial cells (SAEC-hTERT) following 6 month in vitro chronic exposure to six separate treatments to assess differences in carbon nanotube (CNT) vs. asbestos potential tumorigenesis signaling. Dispersed single wall CNT (D-SWCNT), multi-wall CNT (D-MWCNT), ultrafine carbon black (D-UFCB), crocidolite asbestos (ASB) and saline (SAL) exposed cells were compared to SurvantaM-BM-. dispersant (DISP) passage control cells. Each treatment possessed 3 biological cDNA replicates. One technical replicate was performed per biological sample.
2013-07-22 | E-GEOD-41178 | biostudies-arrayexpress
Project description:Recent in vivo studies reported that inhaled carbon nanotube distribute in the alveolar region resulting in an acute inflammation, progressive fibrotic response and particle accumulation at the bronchoalveolar junction with low clearance. With similar biopersistence and shape as asbestos, a known lung carcinogen, growing concern has arisen for elevated risk of carbon nanotube-induced lung carcinogenesis; however few studies have evaluated long-term human health risks associated with chronic pulmonary carbon nanotube exposures compared to asbestos. To address this knowledge gap, we conducted subchronic in vitro exposures of dispersed single walled carbon nanotube, multi-walled carbon nanotube and crocidolite asbestos to human small airway epithelial cells to assess their neoplastic transformation potential. Subchronic single-, multi-walled carbon nanotube and asbestos exposures caused human lung cell neoplastic transformation exhibited by increased proliferation, anchorage-independent growth, invasion and angiogenesis. Whole genome profiling and protein expression analyses showed that carbon nanotube-induced transformation mechanism(s) was largely different from asbestos-related inflammatory signaling, suggesting specific carbon nanotube-induced carcinogenic potential. This study provides novel carbon nanotube and asbestos toxicogenomic information for risk assessment and an in vitro model to evaluate transformation potential of carbon nanotubes and other nanoparticles.
2013-07-22 | GSE41178 | GEO
Project description:There is a current interest in reducing the in vivo toxicity testing of nanomaterials in animals by increasing toxicity testing using in vitro cellular assays; however, toxicological results are seldom concordant between in vivo and in vitro models. This study compared global multi-walled carbon nanotube (MWCNT)-induced gene expression from human lung epithelial and microvascular endothelial cells in monoculture and coculture with gene expression from mouse lungs exposed to MWCNT. Using a cutoff of 10% false discovery rate and 1.5 fold change, we determined that there were more concordant genes (gene expression both up- or downregulated in vivo and in vitro) expressed in both cell types in coculture than in monoculture. When reduced to only those genes involved in inflammation and fibrosis, known outcomes of in vivo MWCNT exposure, there were more disease-related concordant genes expressed in coculture than monoculture. Additionally, different cellular signaling pathways are activated in response to MWCNT dependent upon culturing conditions. As coculture gene expression better correlated with in vivo gene expression, we suggest that cellular cocultures may offer enhanced in vitro models for nanoparticle risk assessment and the reduction of in vivo toxicological testing.
2019-04-12 | GSE129640 | GEO
Project description:coculture SAEC and HMVEC exposed to MWCNT
| PRJNA542679 | ENA
Project description:Adverse lung effects in rodents following pulmonary exposure to multi-walled carbon nanotubes (MWCNT) are well documented. However, systemic effects are less understood. Prospective epidemiological studies have shown increased cardiovascular disease risk after pulmonary exposure to airborne particles, which has led to concerns that inhalation exposure to MWCNT might pose similar risks. We used high-content genomics tools to compare hepatic responses after exposure to a short, entangled MWCNT to the hepatic responses after exposure to a long, stiffer MWCNT at the global transcriptomic level. Female C57BL/6 mice were exposed by single intratracheal instillation to 162 M-BM-5g/mouse of a short MWCNT (NRCWE-26 (NC-7000), 847M-BM-1102 nm in length) or long MWCNT (NM-401 (CP-0006-SG), 4048M-BM-1366 nm in length). Liver tissues were harvested 24 h, 3 d and 28 d after exposure. This experiment examined the pulmonary transcriptional response of female C57BL/6 mice exposed to NRCWE-26, a short multi-walled carbon nanotube, and NM-401, a long multi-walled carbon nanotube, at three doses: D1 (18 M-NM-<g), D2 (54 M-NM-<g), D3 (162 M-NM-<g), and vehicle control. Each dose group was examined 1, 3 or 28 days post-exposure. Each dose group had 6 biological replicates. There were a total of 72 samples included in the final analysis using a two-color reference design.
2015-02-02 | E-GEOD-61366 | biostudies-arrayexpress
Project description:Multi-walled carbon nanotubes (MWCNT) cause lung fibrosis in rodents and exacerbate airway fibrosis in the mouse ovalbumin model of allergic asthma. Interleukin 13 (IL-13) is a key cytokine secreted by T helper type 2 (Th2) cells. IL-13 is up-regulated in human asthma and animal models that activate pro-fibrotic and pro-proliferative cell signaling cascades in human lung fibroblasts (HLF). This study tested the hypothesis that IL-13 alters the gene expression profile of HLF exposed to MWCNT. Carbon black nanoparticles (CBNP) were also compared to MWCNT as they are relatively inert nanoparticles that do not cause fibrosis. Confluent, quiescent cultures of HLF were treated with 10 ng/ml IL-13 or serum-free defined medium (vehicle) for 24 hours prior to treatment with 10 M-BM-5g/cm2 MWCNT or CBNP. At 4, 24, or 48 hours following nanoparticle exposure, total RNA was isolated and gene expression was measured using the Affymetrix Human Genome U133A2.0 Array. The data were analyzed using the JMP Genomics statistical platform. IL-13 and MWCNT each caused changes in the expression of distinct gene subsets over the time-course investigated. The combination of IL-13 and MWCNT resulted in a gene expression profile that was distinct from patterns induced or suppressed by either IL-13 or MWCNT alone. CBNP caused changes in gene expression that were distinct from IL-13 or MWCNT. Interestingly, the combination of IL-13 and MWCNT increased the expression of IL-17A and increased collagen (Col1A1), while MWCNT alone increased interferon-inducible protein-27 (IFI27), suggesting that Th2 microenvironment containing IL-13 shifts MWCNT-induced gene expression from a Th1 to a Th17 gene expression profile. These data provide insight into the mechanisms by which MWCNT alter the biology of fibroblasts during normal and allergic inflammatory conditions. Adult Lung Fibroblasts were treated with 10 M-BM-5g/cm2 MWCNT, CBNP, or vehicle with or without IL-13 for 4 hours, 24 hours, or 48 hours.
2013-05-29 | E-GEOD-43515 | biostudies-arrayexpress
Project description:Multi-walled carbon nanotubes (MWCNTs) are extensively produced and used in composite materials and electronic applications, thus increasing risk of worker and consumer exposure. MWCNTs are an inhomogeneous group of nanomaterials that exist in various lengths, shapes and with different metal compositions, which makes hazard evaluation difficult. However, several studies suggest that length plays an important role in the toxicity induced by MWCNTs. How the length influences toxicity at the molecular level is yet to be characterized. We used high-content genomics tools to compare pulmonary responses after exposure to a short, entangled MWCNT to the pulmonary responses after exposure to a long, stiffer MWCNT at the global transcriptomic level. Female C57BL/6 mice were exposed by single intratracheal instillation to 18, 54 or 162 M-BM-5g/mouse of a short MWCNT (NRCWE-26 (NC-7000), 847M-BM-1102 nm in length) or long MWCNT (NM-401 (CP-0006-SG), 4048M-BM-1366 nm in length). Lung tissues were harvested 24 h, 3 d and 28 d after exposure. This experiment examined the pulmonary transcriptional response of female C57BL/6 mice exposed to NRCWE-26, a short multi-walled carbon nanotube, and NM-401, a long multi-walled carbon nanotube, at three doses: D1 (18 M-NM-<g), D2 (54 M-NM-<g), D3 (162 M-NM-<g), and vehicle control. Each dose group was examined 1, 3 or 28 days post-exposure. Each dose group had 5-6 biological replicates. There were a total of 139 samples included in the final analysis using a two-color reference design.
2015-02-18 | E-GEOD-55286 | biostudies-arrayexpress
Project description:Multi-walled carbon nanotubes (MWCNT) cause lung fibrosis in rodents and exacerbate airway fibrosis in the mouse ovalbumin model of allergic asthma. Interleukin 13 (IL-13) is a key cytokine secreted by T helper type 2 (Th2) cells. IL-13 is up-regulated in human asthma and animal models that activate pro-fibrotic and pro-proliferative cell signaling cascades in human lung fibroblasts (HLF). This study tested the hypothesis that IL-13 alters the gene expression profile of HLF exposed to MWCNT. Carbon black nanoparticles (CBNP) were also compared to MWCNT as they are relatively inert nanoparticles that do not cause fibrosis. Confluent, quiescent cultures of HLF were treated with 10 ng/ml IL-13 or serum-free defined medium (vehicle) for 24 hours prior to treatment with 10 µg/cm2 MWCNT or CBNP. At 4, 24, or 48 hours following nanoparticle exposure, total RNA was isolated and gene expression was measured using the Affymetrix Human Genome U133A2.0 Array. The data were analyzed using the JMP Genomics statistical platform. IL-13 and MWCNT each caused changes in the expression of distinct gene subsets over the time-course investigated. The combination of IL-13 and MWCNT resulted in a gene expression profile that was distinct from patterns induced or suppressed by either IL-13 or MWCNT alone. CBNP caused changes in gene expression that were distinct from IL-13 or MWCNT. Interestingly, the combination of IL-13 and MWCNT increased the expression of IL-17A and increased collagen (Col1A1), while MWCNT alone increased interferon-inducible protein-27 (IFI27), suggesting that Th2 microenvironment containing IL-13 shifts MWCNT-induced gene expression from a Th1 to a Th17 gene expression profile. These data provide insight into the mechanisms by which MWCNT alter the biology of fibroblasts during normal and allergic inflammatory conditions.
2013-05-29 | GSE43515 | GEO
Project description:In order to evaluate the identification of genes and pathways, the global gene expression profiles were assessed in response to multiwall carbon nanotube (MWCNT) on the soil nematode, Caenorhabditis elegans. We performed whole genome DNA microarray experiments with subsequent quantitative analysis conducted on selected genes.
2011-12-31 | GSE24847 | GEO