Genomic approach to explore altered signaling networks of olfaction in response to diesel exhaust particles in mice
Autor: | Moo Kyun Park, Su Ji Kim, Young Rok Seo, An Soo Jang, Nahyun Kim, Jae Jun Song, Bu Soon Son, Hyun Soo Kim, So Hyeon Park |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Microarray Neurite Interleukin-1beta Synaptophysin Gene Expression lcsh:Medicine Sensory system Olfaction Biology complex mixtures Article Olfaction Disorders 03 medical and health sciences 0302 clinical medicine Sniffing medicine Animals lcsh:Science Vehicle Emissions Mice Inbred BALB C Multidisciplinary Interleukin-6 Regeneration (biology) lcsh:R Health care Neurotoxicity Environmental Exposure Retinoic Acid 4-Hydroxylase respiratory system Microarray Analysis medicine.disease Smell Environmental sciences Cytoskeletal Proteins Biomarker 030104 developmental biology Neurology Female Particulate Matter lcsh:Q Neuroscience 030217 neurology & neurosurgery Signal Transduction |
Zdroj: | Scientific Reports, Vol 10, Iss 1, Pp 1-10 (2020) Scientific Reports |
ISSN: | 2045-2322 |
Popis: | Airborne pollutants have detrimental effect on the human body and the environment. Diesel exhaust particles (DEPs) are known to be major component of particulate matter (PM) and cause respiratory diseases and neurotoxicity. However, the effects of air pollutants on the sensory nervous system, especially on the olfactory sense, have not been well studied. Herein, we aimed to explore DEP-induced changes in the olfactory perception process. Olfactory sensitivity test was performed after DEP inhalation in mice. Microarray was conducted to determine the differentially expressed genes, which were then utilized to build a network focused on neurotoxicity. Exposure to DEPs significantly reduced sniffing in mice, indicating a disturbance in the olfactory perception process. Through network analysis, we proposed five genes (Cfap69, Cyp26b1, Il1b, Il6, and Synpr) as biomarker candidates for DEP-mediated olfactory dysfunction. Changes in their expression might provoke malfunction of sensory transduction by inhibiting olfactory receptors, neurite outgrowth, and axonal guidance as well as lead to failure of recovery from neuroinflammatory damage through inhibition of nerve regeneration. Thus, we suggest the potential mechanism underlying DEPs-mediated olfactory disorders using genomic approach. Our study will be helpful to future researchers to assess an individual’s olfactory vulnerability following exposure to inhalational environmental hazards. |
Databáze: | OpenAIRE |
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