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        Identification of novel potential biomarkers and signaling pathways related to otitis media induced by diesel exhaust particle in in vivo system via transcriptomic analysis
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        Identification of novel potential biomarkers and signaling pathways related to otitis media induced by diesel exhaust particle in in vivo system via transcriptomic analysis
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        Identification of novel potential biomarkers and signaling pathways related to otitis media induced by diesel exhaust particle in in vivo system via transcriptomic analysis
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Learning Objectives: The aim of the present study was to discover potential molecular biomarkers and pathways triggered by DEP exposure in rodent model. Here, we conducted transcriptomic analysis to identify novel potential biomarkers in middle ears of DEP-exposed mice.

Introduction: Association between air pollutants and inflammatory diseases such as Otitis Media (OM) has been shown in recent studies. Diesel exhaust particle (DEP), one of major components among diverse air pollutants, is characterized by a carbonic mixture composed of polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, small amounts of sulfate, nitrate, metals, and other trace elements. The exposure to DEP as a risk factor for inflammatory diseases has been reported in several recent investigations. In line with these, our previous study identified potential biomarkers in in vitro system through gene expression microarray and pathway analysis. Although investigations in in vitro system have been conducted to elucidate plausible biomarkers and molecular mechanisms related with DEP, it is necessary to carry out in vivo study to identify exact biological relevance regarding incidence of OM caused by DEP exposure.

Methods: We conducted transcriptomic analysis to identify novel potential biomarkers in middle ears of DEP-exposed mice.

Results: A total of 697 genes were differentially expressed in the DEP-exposed mice; 424 genes and 273 genes were up-and down-regulated, respectively. In addition, signaling pathways among differentially expressed genes mediated by DEP exposure were predicted from different two point of view. Subsequently, we identified several key molecular biomarkers, CHRM1, EPO, SOS1, ESR1, CD4, and IFNA1.

Conclusions: In conclusion, our results might ascertain related cell process and signaling interacted genes underlying DEP exposure and its effects. Moreover, the discovered biomarkers can be recognized as potential candidates for developing early diagnosis and effective treatment strategies of DEP-mediated disorders.

Learning Objectives: We discovered potential molecular biomarkers and pathways triggered by DEP exposure in rodent model.