Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of mouse Apoe knockouts treated with SRM2975 and C57Bl/6 mice treated with exhaust particles reveals Serum amyloid and serum amyloid P are not induced in response to diesel exhaust particles or carbon black

ABSTRACT: W evaluated an experimental particle exposure model, including markers of the acute phase system assessed as the hepatic mRNA expression of Sap, the murine homologue of CRP, and Saa1 and Saa3. Experiment Overall Design: 12-13 weeks old Apoe knockout mice (C57BL/6-Apoe tm1) mice were injected intraperitoneally with varying doses of SRM 2975. In a parallel experiment C57BL mice were exposed by inhalation for 90 minutes to four consecutive doses of 20mg/m3 of filtered air, NIST 2975 or Ptintex 90. Livers and aortic tissue were collected.

ORGANISM(S): Mus musculus

SUBMITTER: Andrew Williams

PROVIDER: E-GEOD-11346 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Lack of acute phase response in the livers of mice exposed to diesel exhaust particles or carbon black by inhalation.

Saber Anne T AT Halappanavar Sabina S Folkmann Janne K JK Bornholdt Jette J Boisen Anne Mette Z AM Møller Peter P Williams Andrew A Yauk Carole C Yauk Carole C Vogel Ulla U Loft Steffen S Wallin Håkan H

Particle and fibre toxicology 20090420

<h4>Background</h4>Epidemiologic and animal studies have shown that particulate air pollution is associated with increased risk of lung and cardiovascular diseases. Although the exact mechanisms by which particles induce cardiovascular diseases are not known, studies suggest involvement of systemic acute phase responses, including C-reactive protein (CRP) and serum amyloid A (SAA) in humans. In this study we test the hypothesis that diesel exhaust particles (DEP) - or carbon black (CB)-induced l ...[more]

PMID: 19374780

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Project description:In the present study we investigate the effect of maternal pulmonary exposure to titanium dioxide (UV-Titan designed for use in the paint and lacquer industry) on prenatally exposed offspring. Time-mated mice (C57BL/6BomTac) were exposed by inhalation for 1 h/day to 42 mg UV-titan/m3 aerosolized powder or filtered air during gestation days (GD) 8-18. We evaluated levels of DNA strand breaks using the comet assay in bronchioalveolar lavage (BAL) cells and liver cells of the time-mated mice, and in liver cells of the offspring. In parallel, we analyzed changes in gene expression in the liver tissue of offspring using DNA microarrays. We demonstrate that UV-Titan did not induce DNA strand breaks in the time-mated mice or their offspring. Transcriptional profiling of newborn liver tissue revealed changes in the expression of genes related to the retinoic acid (RA) signalling pathway in the females, while gene expression in male offspring was relatively unaffected by exposure. Time-mated, nulliparous mice (C57BL/6BomTac, Taconic Europe, Ejby, Denmark) were exposed to filtered clean air or approximately 42 mg/m3 UV-Titan on GD 8M-bM-^@M-^S18 for 1 hr/day by a whole-body exposure.Delivery was expected on GD 20, and designated postnatal day (PND) 0. On PND 2, one offspring (M-bM-^@M-^\newbornM-bM-^@M-^]) per litter was killed by decapitation, to yield litters with at least 5 offspring per exposure group. The newborn offspring were collected two days after birth. On PND 23-24 (M-bM-^@M-^\at weaningM-bM-^@M-^]) one male and one female per litter were killed. Organs were dissected, weighed, placed in NUNC cryotubes, snap frozen in liquid N2 and stored at -80M-BM-0C until analysis. Exposed dams were killed on PND 24-25 (26-27 days after last exposure). DNA strad break detection was carried out in bronchoalveolar lavage fluid in dams by COMET assay. Total RNA was extracted from offspring livers and gene expression profiling was carried out on whole liver tissues from offspring. 9 UV-Titan treated and 7 controls mice consisting of 8 males and 8 females mRNA, hepatic, developmental, Toxicogenomics, nano-titanium dioxide

Dataset Information

Transcription profiling of mouse Apoe knockouts treated with SRM2975 and C57Bl/6 mice treated with exhaust particles reveals Serum amyloid and serum amyloid P are not induced in response to diesel exhaust particles or carbon black

Publications

Lack of acute phase response in the livers of mice exposed to diesel exhaust particles or carbon black by inhalation.

Similar Datasets

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