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miRNA-6515-5p regulates particulate matter-induced inflammatory responses by targeting CSF3 in human bronchial
Eun Suk Son1, Ui Won Ko2, Hee-Yeon Jeong2
1Department of Medicine, College of Medicine, Gachon University, Incheon, Republic of Korea.
Abstract:
Particulate matter (PM) is associated with the incidence, exacerbation, and mortality of variable respiratory diseases. However, the molecular mechanisms of PM10-mediated inflammation are unclear. We identified microRNAs (miRNAs) and messenger RNAs (mRNAs) related to the inflammatory response in PM10-exposed bronchial epithelial cells using next-generation sequencing. Of the miRNAs, miR-6515-5p was significantly downregulated in PM10-exposed human bronchial epithelial BEAS-2B cells. miR-6515-5p regulated the production of pro-inflammatory cytokines (IL-6 and IL-8) and the expression of inflammatory genes (IL-1β, IL-6, IL-8, TNF-α, CXCL-1, and MCP-1) via MAPK/ERK signaling; overexpression of miR-6515-5p using a mimic inhibited PM10-induced inflammatory responses via inactivation of the ERK pathway, whereas downregulation of miR-6515-5p via an inhibitor significantly increased inflammation in PM10-exposed cells via activation of ERK. Furthermore, we identified colony stimulating factor 3 (CSF3) as a target gene of miR-6515-5p using TargetScanHuman, and confirmed the association between miR-6515-5p and CSF3 using a luciferase reporter assay. Furthermore, we found that mRNA and protein levels of CSF3 were negatively regulated by miR-6515-5p. Inhibition of CSF3 by small interfering RNA significantly reduced the expression and production of inflammatory markers in PM10-exposed cells by inactivating the MAPK/ERK signaling pathway. Therefore, we suggest that miR-6515-5p regulates PM10-induced inflammatory responses by targeting CSF3 via MAPK/ERK signaling in bronchial epithelial cells.
Insights
Particulate matter (PM10) triggers respiratory inflammation by downregulating miR-6515-5p. This microRNA targets CSF3, inhibiting the MAPK/ERK pathway and reducing inflammatory responses in bronchial cells.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Environmental Health
Background:
- Particulate matter (PM) exposure is linked to respiratory diseases, but its precise molecular inflammatory mechanisms remain elusive.
- Understanding the role of microRNAs (miRNAs) in PM-induced inflammation is crucial for developing targeted therapies.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying PM10-mediated inflammation in bronchial epithelial cells.
- To identify key miRNAs and their target genes involved in the inflammatory response to PM10.
Main Methods:
- Next-generation sequencing to identify differentially expressed miRNAs and mRNAs in PM10-exposed bronchial cells.
- miRNA mimic and inhibitor transfections to modulate miR-6515-5p levels.
- Luciferase reporter assays to confirm target gene interactions.
- Small interfering RNA (siRNA) to inhibit target gene expression.
Main Results:
- PM10 exposure significantly downregulated miR-6515-5p in human bronchial epithelial cells (BEAS-2B).
- miR-6515-5p directly targets colony stimulating factor 3 (CSF3), regulating its mRNA and protein levels.
- Overexpression of miR-6515-5p suppressed PM10-induced inflammation via MAPK/ERK pathway inactivation; inhibition exacerbated it via ERK activation.
- Inhibition of CSF3 reduced PM10-induced inflammatory markers by inactivating the MAPK/ERK pathway.
Conclusions:
- miR-6515-5p acts as a crucial regulator of PM10-induced inflammation in bronchial epithelial cells.
- The miR-6515-5p/CSF3 axis modulates inflammatory responses through the MAPK/ERK signaling pathway.
- Targeting this pathway offers a potential therapeutic strategy for PM-related respiratory diseases.
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