MiR-3202 protects smokers from chronic obstructive pulmonary disease through inhibiting FAIM2: An in vivo and in vitro study
- The Third Ward of Respiratory Department, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101 Yunnan Province (China)
- Department of experimental zoology, Kunming Medical University, Kunming, 650101 Yunnan Province (China)
Highlights: • Smoking decreased level of miR-3202 both in COPD patients and normal donors. • The miR-3202 influenced the release of inflammatory factors through targeting FAIM2 in T lymphocytes. • Abnormal expression of miR-3202 in T lymphocytes damaged human bronchial epithelial cells. Previous study found the variable miR-3202 as a potential biomarker in smoker with or without chronic obstructive pulmonary disease (COPD). This study aims to identify the molecular involvement of miR-3202 in the pathophysiology of COPD. Level of miR-3202 in blood sample of non-smoker non-COPD(C), smoker without COPD(S), smoker with stable COPD(S-COPD) and smoker with acute exacerbation COPD(AE-COPD) was observed by quantitative real-time PCR. By bioinformatics prediction, Fas apoptotic inhibitory molecule 2 (FAIM2) was identified as a potential target of miR-3202. In vitro, human bronchial epithelial (HBE) cells and cigarette smoke extract (CSE) stimulated T lymphocytes were co-cultured. Cell proliferation and apoptosis of HBE cells were determinated. In vivo, rats were exposed in cigarette smoke for 30 days and expression of miR-3202 and FAIM2 in bronchia were detected. Results showed that The miR-3202 was down-regulated in S, S-COPD and AE-COPD group when compared with C group. Decreased level of miR-3202 was also observed in CSE treated T lymphocyte. Additionally, CSE stimulation increased INF-γ and TNF-α levels and FAIM2 expression whereas inhibited Fas and FasL expressions in T lymphocytes. However, these effects were significantly suppressed by miR-3202 overexpression and enhanced by miR-3202 inhibitor. Likely to exogenous miR-3202, FAIM2 knockdown significantly inhibited HBE cells apoptosis, as well as inhibited INF-γ and TNF-α levels. In COPD rats model, miR-3202 was reduced while FAIM2 was up-regulated accordingly. Here, results suggest that high level miR-3202 in T lymphocytes may protect epithelial cells through targeting FAIM2. MiR-3202 might be used as a notable biomarker of COPD.
- OSTI ID:
- 23082485
- Journal Information:
- Experimental Cell Research, Vol. 362, Issue 2; Other Information: Copyright (c) 2017 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
- Country of Publication:
- United States
- Language:
- English
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