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Expression of microRNA machinery proteins in different types of chronic rhinosinusitis
Ya-Na Zhang1, Ping-Ping Cao, Xin-Hao Zhang
1Department of Otolaryngology-Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Objectives/Hypothesis:
Dysregulation of microRNAs (miRNAs) has recently been shown in chronic rhinosinusitis (CRS), the biogenesis and function of which are modulated by miRNA machinery proteins. The expression of these proteins in inflammatory airway diseases is unclear. The aim of this study was to investigate the expression of miRNA machinery components in CRS.
Study Design:
Case-control experimental study.
Methods:
The mRNA expression levels of miRNA machinery components including Drosha, Dicer, protein activator of the interferon-induced protein kinase (PACT), human immunodeficiency virus transactivating response RNA-binding protein, fragile X mental retardation protein, and argonaute 2/eukaryotic translation initiation factor 2C, 2 in nasal biopsies from control, CRS without nasal polyps (CRSsNP), eosinophilic, and noneosinophilic CRS with nasal polyps (CRSwNP) subjects were determined by quantitative reverse transcription polymerase chain reaction. Immunohistochemical staining was employed to examine the protein expression of PACT and the cellular source of PACT.
Results:
Among the tested components, only PACT mRNA expression was found to be altered in CRS, the levels of which were upregulated in CRSwNP as compared with control. In comparison with control and CRSsNP, PACT protein expression was also significantly upregulated in CRSwNP, with a further increase in eosinophilic CRSwNP. PACT was mainly expressed in CD138(+) plasma cells. A higher percentage of PACT-positive plasma cells in total plasma cells was detected in eosinophilic CRSwNP than in noneosinophilic CRSwNP. PACT protein expression correlated with disease severity and eosinophil infiltration.
Conclusions:
PACT may be associated with the plasma cell function and eosinophilic inflammation in CRSwNP. However, further experimentation is needed to clarify the functions of PACT.
Insights
MicroRNA machinery protein PACT is upregulated in chronic rhinosinusitis with nasal polyps (CRSwNP), particularly in eosinophilic cases. This suggests PACT may play a role in plasma cell function and eosinophilic inflammation in CRSwNP.
Area of Science:
- Molecular Biology
- Immunology
- Otorhinolaryngology
Background:
- MicroRNA (miRNA) dysregulation is implicated in chronic rhinosinusitis (CRS).
- miRNA biogenesis and function depend on specific machinery proteins.
- The role of these proteins in inflammatory airway diseases like CRS remains largely unknown.
Purpose of the Study:
- To investigate the expression of miRNA machinery components in CRS.
- To determine if specific components are altered in different CRS subtypes.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure mRNA levels of miRNA machinery components in nasal biopsies.
- Immunohistochemical staining assessed protein expression and cellular localization of Protein Activator of the Interferon-induced Protein Kinase (PACT).
- Study included control subjects and patients with CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP), including eosinophilic and noneosinophilic phenotypes.
Main Results:
- Only PACT mRNA expression was significantly altered, showing upregulation in CRSwNP compared to controls.
- PACT protein expression was significantly upregulated in CRSwNP versus controls and CRSsNP, with further elevation in eosinophilic CRSwNP.
- PACT was primarily expressed in CD138(+) plasma cells, with a higher proportion of PACT-positive plasma cells in eosinophilic CRSwNP. PACT protein levels correlated with disease severity and eosinophil infiltration.
Conclusions:
- PACT upregulation in CRSwNP, especially eosinophilic forms, suggests a potential role in plasma cell function and eosinophilic inflammation.
- Further research is warranted to elucidate the precise functions of PACT in the pathogenesis of CRSwNP.