Effect of PM2.5 on MicroRNA Expression and Function in Nasal Mucosa of Rats With Allergic Rhinitis

Abstract

Background Particulate matter 2.5 (PM2.5) refers to particulate matter with aerodynamic equivalent diameter less than or equal to 2.5 µm, which is an important component of air pollution. PM2.5 aggravates allergic rhinitis (AR) and promotes AR nasal mucosa inflammation. Therefore, the influence of PM2.5 inhalation exposure on microRNA (miRNA) expression profiles and function in the nasal mucosa of AR rats was investigated. Methods Female Sprague Dawley rats were distributed randomly to 2 groups: AR model PM2.5 exposure group (ARE group) and AR model PM2.5-unexposed control group (ARC group). The rats of ARE group were made to inhale PM2.5 at a concentration of 200 µg/m3, 3 h/day, for 30 days. miRNA expression profiles of the nasal mucosa from both groups were determined using an miRNA gene chip and were verified by quantitative real-time PCR (qRT-PCR). Gene function enrichment analysis was performed using bioinformatics analysis. Results The ARE group revealed 20 significantly differentially expressed miRNAs, including 4 upregulated and 16 downregulated miRNAs (fold change > 1.5 or < 0.66, P < .05). Of these, 9 selected miRNAs were verified by qRT-PCR, and the results of 8 miRNAs were in accordance with the miRNA gene chip results, with highly positive correlation ( r = .8583, P = .0031). Numerous target genes of differentially expressed miRNAs were functionally enriched in high-affinity immunoglobulin E receptor signaling, ErbB signaling, mucin O-glycans biosynthesis, transforming growth factor β signaling, mitogen-activated protein kinase signal transduction, phosphatidylinositol signaling, mucopolysaccharide biosynthesis, mammalian target of rapamycin signaling, T cell receptor signaling, Wnt signaling, chemokine signal transduction, and natural killer cell-mediated cytotoxicity pathways. Conclusions PM2.5 causes significant changes in miRNA expression in the nasal mucosa of AR rats. miRNA plays an important role in regulating PM2.5 effects in AR rat biological behavior and mucosal inflammation. This study provides a theoretical basis for the prevention and treatment of AR from the effects of environmental pollution on the gene regulation mechanism.

MicroRNA‐214‐3p facilitates M2 macrophage polarization by targeting GSK3B

“…In AR pathogenesis, miR‐202‐5p targets MATN2 to facilitate M2 phenotype polarization 21 . Consistent with a previous study, 19 miR‐214‐3p was found to be overexpressed in nasal mucus tissues and macrophages from AR patients in this study, suggesting that miR‐214‐3p may be associated with AR development. MiR‐214, miR‐145, miR‐544, miR‐138, and miR‐371 can modulate the balance between Type 1 helper T/Type 2 helper T cells by regulating Runx3 in a combinatorial manner in asthma, a disease that can be triggered by AR 26 .…”

“…25 In AR pathogenesis, miR-202-5p targets MATN2 to facilitate M2 phenotype polarization. 21 Consistent with a previous study, 19 miR-214-3p was found to be overexpressed in nasal mucus tissues and macrophages from AR asthma, a disease that can be triggered by AR. 26 Caspase-1 signaling, a pathway regulated by miR-214-3p, 16 has been validated to exert critical functions in AR models.…”

“…15 MiR-214-3p has been reported to be involved in the development of diverse diseases, such as atherosclerosis, 16 osteoarthritis, 17 and recurrent pregnancy loss. 18 Interestingly, miR-214-3p was demonstrated to be overexpressed in nasal mucus tissues from AR patients, 19 which indicates that miR-214-3p may participate in AR development. Nevertheless, the role and specific mechanism of miR-214-3p in AR progression are still uncharacterized.…”

Exposure to Fine Particulate Matter Air Pollution Alters mRNA and miRNA Expression in Bone Marrow-Derived Endothelial Progenitor Cells from Mice

“…Consistent with this idea, we did identify reciprocal relationships between representative dysregulated genes and at least one of their documented, targeting miRNAs ( Table 7 ). Supporting this mechanism of PM 2.5 -induced gene expression changes, other studies also suggested that particle inhalation [ 38 , 39 ] or exposure to particles in cell culture models [ 40 , 41 ] induces the upregulation or downregulation of specific miRNAs. Other epigenetic mechanisms may involve the modification of nuclear material.…”

Staying Safe, Caring for Each Other, and Moving the Needle—Together

“…Researchers share their findings on topical vitamin D modulating human sinonasal mucosal responses to dust mite antigen, 3 the differential expression of long noncoding RNAs and their function-related mRNAs in allergic rhinitis patients, 8 and the effect of PM2.5 on microRNA expression and function in the nasal mucosa of rats with allergic rhinitis. 12 Chen et al 14 also present a thorough review and meta-analysis on barrier protection measures for the management of allergic rhinitis which is very informative. Finally in another systematic review, Lee et al 15 provide a detailed analysis of cystic fibrosis transmembrane conductance regulator modulator therapy which is an excellent overview on this complex topic.…”