Identification of potential novel biomarkers and signaling pathways related to otitis media induced by diesel exhaust particles using transcriptomic analysis in an in vivo system

Hyo Jeong Kim, So Young Kim, Jee Young Kwon, Yeo Jin Kim, Seung Hun Kang, Won Hee Jang, Jun Ho Lee, Myung Whan Seo, Jae-Jun Song, Young Rok Seo, Moo Kyun Park

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Introduction Air pollutants are associated with inflammatory diseases such as otitis media (OM). Significantly higher incidence rates of OM are reported in regions with air pollution. Diesel exhaust particles (DEPs) comprise a major class of contaminants among numerous air pollutants, and they are characterized by a carbonic mixture of polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, and small amounts of sulfate, nitrate, metals and other trace elements. DEP exposure is a risk factor for inflammatory diseases. Our previous study identified potential biomarkers using gene expression microarray and pathway analyses in an in vitro system. Although in vitro investigations have been conducted to elucidate plausible biomarkers and molecular mechanisms related to DEP exposure, in vivo studies are necessary to identify the exact biological relevance regarding the incidence of OM caused by DEP exposure. In this study, we identified potential molecular biomarkers and pathways triggered by DEP exposure in a rodent model. Methods Transcriptomic analysis was employed to identify novel potential biomarkers in the middle ear of DEP-exposed mice. Results A total of 697 genes were differentially expressed in the DEP-exposed mice; 424 genes were upregulated and 273 downregulated. In addition, signaling pathways among the differentially expressed genes mediated by DEP exposure were predicted. Several key molecular biomarkers were identified including cholinergic receptor muscarinic 1 (CHRM1), erythropoietin (EPO), son of sevenless homolog 1 (SOS1), estrogen receptor 1 (ESR1), cluster of differentiation 4 (CD4) and interferon alpha-1 (IFNA1). Conclusions Our results shed light on the related cell processes and gene signaling pathways affected by DEP exposure. The identified biomarkers might be potential candidates for determining early diagnoses and effective treatment strategies for DEP-mediated disorders.

Original languageEnglish
Article numbere0166044
JournalPLoS One
Volume11
Issue number11
DOIs
Publication statusPublished - 2016 Nov 1

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Vehicle Emissions
otitis media
Otitis Media
Biomarkers
transcriptomics
biomarkers
Genes
Air Pollutants
Polycyclic Aromatic Hydrocarbons
polycyclic aromatic hydrocarbons
SOS1 Protein
genes
pollutants
incidence
erythropoietin
air
interferon-alpha
cholinergic receptors
Estrogen Receptor alpha
early diagnosis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

Identification of potential novel biomarkers and signaling pathways related to otitis media induced by diesel exhaust particles using transcriptomic analysis in an in vivo system. / Kim, Hyo Jeong; Kim, So Young; Kwon, Jee Young; Kim, Yeo Jin; Kang, Seung Hun; Jang, Won Hee; Lee, Jun Ho; Seo, Myung Whan; Song, Jae-Jun; Seo, Young Rok; Park, Moo Kyun.

In: PLoS One, Vol. 11, No. 11, e0166044, 01.11.2016.

Research output: Contribution to journalArticle

Kim, Hyo Jeong ; Kim, So Young ; Kwon, Jee Young ; Kim, Yeo Jin ; Kang, Seung Hun ; Jang, Won Hee ; Lee, Jun Ho ; Seo, Myung Whan ; Song, Jae-Jun ; Seo, Young Rok ; Park, Moo Kyun. / Identification of potential novel biomarkers and signaling pathways related to otitis media induced by diesel exhaust particles using transcriptomic analysis in an in vivo system. In: PLoS One. 2016 ; Vol. 11, No. 11.
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abstract = "Introduction Air pollutants are associated with inflammatory diseases such as otitis media (OM). Significantly higher incidence rates of OM are reported in regions with air pollution. Diesel exhaust particles (DEPs) comprise a major class of contaminants among numerous air pollutants, and they are characterized by a carbonic mixture of polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, and small amounts of sulfate, nitrate, metals and other trace elements. DEP exposure is a risk factor for inflammatory diseases. Our previous study identified potential biomarkers using gene expression microarray and pathway analyses in an in vitro system. Although in vitro investigations have been conducted to elucidate plausible biomarkers and molecular mechanisms related to DEP exposure, in vivo studies are necessary to identify the exact biological relevance regarding the incidence of OM caused by DEP exposure. In this study, we identified potential molecular biomarkers and pathways triggered by DEP exposure in a rodent model. Methods Transcriptomic analysis was employed to identify novel potential biomarkers in the middle ear of DEP-exposed mice. Results A total of 697 genes were differentially expressed in the DEP-exposed mice; 424 genes were upregulated and 273 downregulated. In addition, signaling pathways among the differentially expressed genes mediated by DEP exposure were predicted. Several key molecular biomarkers were identified including cholinergic receptor muscarinic 1 (CHRM1), erythropoietin (EPO), son of sevenless homolog 1 (SOS1), estrogen receptor 1 (ESR1), cluster of differentiation 4 (CD4) and interferon alpha-1 (IFNA1). Conclusions Our results shed light on the related cell processes and gene signaling pathways affected by DEP exposure. The identified biomarkers might be potential candidates for determining early diagnoses and effective treatment strategies for DEP-mediated disorders.",
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AU - Kim, Hyo Jeong

AU - Kim, So Young

AU - Kwon, Jee Young

AU - Kim, Yeo Jin

AU - Kang, Seung Hun

AU - Jang, Won Hee

AU - Lee, Jun Ho

AU - Seo, Myung Whan

AU - Song, Jae-Jun

AU - Seo, Young Rok

AU - Park, Moo Kyun

PY - 2016/11/1

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N2 - Introduction Air pollutants are associated with inflammatory diseases such as otitis media (OM). Significantly higher incidence rates of OM are reported in regions with air pollution. Diesel exhaust particles (DEPs) comprise a major class of contaminants among numerous air pollutants, and they are characterized by a carbonic mixture of polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, and small amounts of sulfate, nitrate, metals and other trace elements. DEP exposure is a risk factor for inflammatory diseases. Our previous study identified potential biomarkers using gene expression microarray and pathway analyses in an in vitro system. Although in vitro investigations have been conducted to elucidate plausible biomarkers and molecular mechanisms related to DEP exposure, in vivo studies are necessary to identify the exact biological relevance regarding the incidence of OM caused by DEP exposure. In this study, we identified potential molecular biomarkers and pathways triggered by DEP exposure in a rodent model. Methods Transcriptomic analysis was employed to identify novel potential biomarkers in the middle ear of DEP-exposed mice. Results A total of 697 genes were differentially expressed in the DEP-exposed mice; 424 genes were upregulated and 273 downregulated. In addition, signaling pathways among the differentially expressed genes mediated by DEP exposure were predicted. Several key molecular biomarkers were identified including cholinergic receptor muscarinic 1 (CHRM1), erythropoietin (EPO), son of sevenless homolog 1 (SOS1), estrogen receptor 1 (ESR1), cluster of differentiation 4 (CD4) and interferon alpha-1 (IFNA1). Conclusions Our results shed light on the related cell processes and gene signaling pathways affected by DEP exposure. The identified biomarkers might be potential candidates for determining early diagnoses and effective treatment strategies for DEP-mediated disorders.

AB - Introduction Air pollutants are associated with inflammatory diseases such as otitis media (OM). Significantly higher incidence rates of OM are reported in regions with air pollution. Diesel exhaust particles (DEPs) comprise a major class of contaminants among numerous air pollutants, and they are characterized by a carbonic mixture of polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, and small amounts of sulfate, nitrate, metals and other trace elements. DEP exposure is a risk factor for inflammatory diseases. Our previous study identified potential biomarkers using gene expression microarray and pathway analyses in an in vitro system. Although in vitro investigations have been conducted to elucidate plausible biomarkers and molecular mechanisms related to DEP exposure, in vivo studies are necessary to identify the exact biological relevance regarding the incidence of OM caused by DEP exposure. In this study, we identified potential molecular biomarkers and pathways triggered by DEP exposure in a rodent model. Methods Transcriptomic analysis was employed to identify novel potential biomarkers in the middle ear of DEP-exposed mice. Results A total of 697 genes were differentially expressed in the DEP-exposed mice; 424 genes were upregulated and 273 downregulated. In addition, signaling pathways among the differentially expressed genes mediated by DEP exposure were predicted. Several key molecular biomarkers were identified including cholinergic receptor muscarinic 1 (CHRM1), erythropoietin (EPO), son of sevenless homolog 1 (SOS1), estrogen receptor 1 (ESR1), cluster of differentiation 4 (CD4) and interferon alpha-1 (IFNA1). Conclusions Our results shed light on the related cell processes and gene signaling pathways affected by DEP exposure. The identified biomarkers might be potential candidates for determining early diagnoses and effective treatment strategies for DEP-mediated disorders.

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