Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of mouse lung response to HDI

ABSTRACT: C57BL/6J mouse were exposed to 10 mg/m3 of aerosolic HDI-BT (hexamethylene diisocyanate biuret trimer) and followed at 6h, 18h, and 90h after exposure together with unexposed mice. Whole lungs were collected for RNA (4 mice for each group, RNA pooled).

ORGANISM(S): Mus musculus

SUBMITTER: Joni Ylostalo

PROVIDER: E-GEOD-1811 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gene expression profiling in mouse lung following polymeric hexamethylene diisocyanate exposure.

Lee Chun-Ting CT Ylostalo Joni J Friedman Mitchell M Hoyle Gary W GW

Toxicology and applied pharmacology 20041118 1

Isocyanates are a common cause of occupational lung disease. Hexamethylene diisocyanate (HDI), a component of polyurethane spray paints, can induce respiratory symptoms, inflammation, lung function impairment, and isocyanate asthma. The predominant form of HDI in polyurethane paints is a nonvolatile polyisocyanate known as HDI biuret trimer (HDI-BT). Exposure of mice to aerosolized HDI-BT results in pathological effects, including pulmonary edema, lung inflammation, cellular proliferation, and f ...[more]

PMID: 15885264

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Project description:Atypical teratoid/rhabdoid tumor (ATRT) is a highly malignant CNS neoplasm whichprimarily occurs in children under three years of age. Due to poor outcomes with intense and toxicmultimodality treatment, new therapies are urgently needed. Histone deacetylase inhibitors (HDIs)have been evaluated as novel agents for multiple malignancies and have been shown to function asradiosensitizers. They act as epigenetic modifiers and lead to re-expression of inappropriatelyrepressed genes, proteins, and cellular functions. Due to the underlying chromatin remodeling genemutation in ATRT, HDIs are ideal candidates for therapeutic evaluation. To evaluate the role of HDIsagainst ATRT in vitro, we assessed the effect of drug treatment on proliferation, apoptosis, and geneexpression. Additionally, we examined HDI pretreatment as a radiosensitization strategy for ATRT.MTS and clonogenic assays demonstrated that HDI treatment significantly reduces the proliferativecapacity of BT-12 and BT-16 ATRT cells. Also, the HDI SNDX-275 was able to induce apoptosis in bothcell lines and induced p21Waf1/Cip1 protein expression as measured by Western blot. Evaluation ofdifferential gene expression by microarray and pathway analysis after HDI treatment demonstratedalterations of several key ATRT cellular functions. Finally, we showed that HDI pretreatmenteffectively potentiates the effect of ionizing radiation on ATRT cells as measured by clonogenic assay.These findings suggest that the addition of HDIs to ATRT therapy may prove beneficial, especiallywhen administered in combination with current treatment modalities such as radiation. Keywords: ATRT; HDAC inhibitor; radiosensitization BT12 and BT16 cells were plated and subsequently treated for 24hr with IC25 concentrations of SNDX-275 (Sigma), at which time total RNA was collected. IC25 concentrations were calculated based on MTS assay.For BT12, the SNDX-275 IC25 was 1.4uM. For BT16, it was 0.44uM. The controls had DMSO added at equivalent volumes.

Dataset Information

Transcription profiling of mouse lung response to HDI

Publications

Gene expression profiling in mouse lung following polymeric hexamethylene diisocyanate exposure.

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