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Published on: March 29, 2017
Mir-142-3p Regulates Inflammatory Response by Contributing to Increased TNF-α in Chronic Rhinosinusitis With Nasal
Xiang Qing1, Yongquan Zhang1, Ya Peng2
1Department of Otorhinolaryngology Head and Neck Surgery, Third Xiangya Hospital, Central South University, Changsha, China.
Objective:
Previous studies suggested that microRNAs played an important role in the progression of inflammation and remodeling of chronic rhinosinusitis with nasal polyposis. However, the abnormal expression of microRNAs and regulation cytokine expression in nasal polyposis are not clear.
Method:
The miR-142-3p and tumor necrosis factor α (TNF-α) expression levels in chronic rhinosinusitis with nasal polyposis were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The miR-142-3p and TNF-α levels in human nasal epithelial cells (HNEpC) after stimulation by lipopolysaccharide (LPS) were detected by qRT-PCR. Moreover, HNEpCs were transfected by miR-142-3p mimics or inhibitor or cotransfected with si-TNF-α to evaluate the regulation of miR-142-3p on TNF-α which affects the production of inflammatory factors.
Results:
The miR-142-3p and TNF-α were significantly higher in nasal mucosa of chronic rhinosinusitis with polyps patients compared to normal human. MiR-142-3p and TNF-α expression levels were increased after LPS stimulation in a dose- and time-dependent manner. Knockdown of miR-142-3p in HNEpCs downregulated TNF-α expression at both messenger RNA and protein levels.
Conclusions:
It is indicated that miR-142-3p may participate in the regulation of the body's inflammatory response through the LPS-TLR-TNF-α signaling pathway in chronic rhinosinusitis with nasal polyposis.
Insights
MicroRNA-142-3p and tumor necrosis factor-alpha are elevated in chronic rhinosinusitis with nasal polyposis. MiR-142-3p may regulate inflammation via the LPS-TLR-TNF-α pathway.
Area of Science:
- Immunology
- Molecular Biology
- Otolaryngology
Background:
- MicroRNAs (miRNAs) are implicated in chronic rhinosinusitis with nasal polyposis (CRSwNP) inflammation and tissue remodeling.
- The specific roles of miRNAs and their regulation of cytokines in CRSwNP remain unclear.
Purpose of the Study:
- To investigate the expression of miR-142-3p and tumor necrosis factor-alpha (TNF-α) in CRSwNP.
- To elucidate the regulatory relationship between miR-142-3p and TNF-α in human nasal epithelial cells (HNEpCs).
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure miR-142-3p and TNF-α levels in CRSwNP tissues and HNEpCs.
- HNEpCs were stimulated with lipopolysaccharide (LPS) and transfected with miR-142-3p mimics/inhibitors or si-TNF-α to assess regulatory effects.
Main Results:
- Both miR-142-3p and TNF-α were significantly upregulated in CRSwNP tissues compared to normal controls.
- LPS stimulation increased miR-142-3p and TNF-α expression in HNEpCs in a dose- and time-dependent manner.
- Downregulation of miR-142-3p reduced TNF-α expression at both mRNA and protein levels in HNEpCs.
Conclusions:
- miR-142-3p is upregulated in CRSwNP.
- miR-142-3p may play a role in CRSwNP pathogenesis by regulating TNF-α.
- The LPS-TLR-TNF-α signaling pathway is implicated in miR-142-3p-mediated inflammation in CRSwNP.
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