MiR-29b-3p promotes particulate matter-induced inflammatory responses by regulating the C1QTNF6/AMPK pathway
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Published on: September 12, 2019
Jian Wang1, Mengchan Zhu1, Ling Ye1
1Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai 200030, China.
Abstract:
Inflammatory responses are considered to be the critical mechanism underlying particulate matter (PM)-induced development and exacerbation of chronic respiratory diseases. MiR-29b-3p has been found to participate in various biological processes, but its role in PM-induced inflammatory responses was previously unknown. Here, we constructed a miRNA PCR array to find that miR-29b-3p was the most highly expressed in human bronchial epithelial cells (HBECs) exposed to PM. MiR-29b-3p promoted PM-induced pro-inflammatory cytokines (IL-1β, IL-6, and IL-8) expression via inhibiting the AMPK signaling pathway in HBECs. RNA sequencing and luciferase reporter assay identified that miR-29b-3p targeted complement C1q tumor necrosis factor-related protein 6 (C1QTNF6), a protein that protected from PM-induced inflammatory responses via activating the AMPK signaling pathway. In vivo, miR-29b-3p antagomirs delivered via the tail vein prior to PM exposure significantly counteracted PM-induced miR-29b-3p upregulation and C1QTNF6 downregulation in lung tissues. Furthermore, miR-29b-3p inhibition alleviated inflammatory cells infiltration and pro-inflammatory cytokines secretion in the lung of PM-exposed mice. These findings firstly revealed that miR-29b-3p acted as a novel modulator of PM-induced inflammatory responses by targeting the C1QTNF6/AMPK signaling pathway, which contributes to a better understanding of the biological mechanisms underlying adverse PM-induced respiratory health effects.
Insights
Particulate matter exposure triggers inflammation in respiratory diseases. This study reveals miR-29b-3p promotes this inflammation by targeting C1QTNF6 and inhibiting the AMPK pathway, offering new therapeutic insights.
Area of Science:
- Environmental Health
- Molecular Biology
- Immunology
Background:
- Particulate matter (PM) exposure is a major driver of chronic respiratory diseases, primarily through inflammatory mechanisms.
- The specific role of microRNAs (miRNAs), like miR-29b-3p, in PM-induced inflammation remained largely unexplored.
Purpose of the Study:
- To investigate the role of miR-29b-3p in particulate matter-induced inflammatory responses in the respiratory system.
- To elucidate the molecular mechanism by which miR-29b-3p influences PM-induced inflammation.
Main Methods:
- Utilized miRNA PCR array to identify upregulated miRNAs in human bronchial epithelial cells (HBECs) exposed to PM.
- Employed RNA sequencing and luciferase reporter assays to identify miR-29b-3p targets.
- Administered miR-29b-3p antagomirs in a mouse model of PM exposure for in vivo validation.
Main Results:
- miR-29b-3p was significantly upregulated in PM-exposed HBECs and promoted pro-inflammatory cytokine (IL-1β, IL-6, IL-8) expression.
- miR-29b-3p targets C1QTNF6, a protein that normally activates the AMPK pathway to protect against PM-induced inflammation.
- In vivo inhibition of miR-29b-3p counteracted PM-induced inflammation, cytokine release, and inflammatory cell infiltration in mouse lungs.
Conclusions:
- miR-29b-3p acts as a novel pro-inflammatory regulator in particulate matter exposure.
- The miR-29b-3p/C1QTNF6/AMPK signaling pathway is a critical mechanism in PM-induced respiratory inflammation.
- Targeting miR-29b-3p presents a potential therapeutic strategy for mitigating adverse respiratory health effects of PM exposure.
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