LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis.

AIMS: Chronic obstructive pulmonary disease (COPD) is a systemic disease. Several long non-coding RNAs (lncRNAs) have been identified to be aberrantly expressed in COPD patients. This study investigated the role of lncRNA cancer susceptibility candidate 2 (CASC2) in COPD, as well as its potential mechanism. METHODS: Fifty smokers with COPD and another 50 smokers without COPD were recruited. Receiver operating characteristic curve was constructed to assess the diagnostic value of CASC2 in COPD patients. 16HBE cells were treated with cigarette smoke extract (CSE) to establish a cell model. qRT-PCR was used for the measurement of mRNA levels. The cell viability and apoptosis were detected by using Cell Counting Kit-8 and flow cytometry assay. Enzyme-linked immunosorbent assay was performed to detect the levels of proinflammatory cytokines. Luciferase reporter assay was performed for the target gene analysis. RESULTS: Serum CASC2 was dramatically decreased in COPD patients compared with smokers without COPD, and was positively associated with FEV1 (forced expiratory volume in one second). Serum CASC2 was overexpressed in severe COPD patients, and had the diagnostic accuracy to distinguish COPD patients from smokers. CASC2 overexpression alleviated CSE-induced apoptosis and inflammation in 16HBE cells. CASC2 functions as a ceRNA of miR-18a-5p. Upregulation of miR-18a-5p reversed the influence of CASC2 on cell apoptosis and inflammation in 16HBE cells. IGF1 was the target gene of miR-18a-5p. CONCLUSION: CASC2 was downregulated in COPD patients and it might be a promising biomarker for the disease diagnosis. Overexpression of CASC2 might inhibit the bronchial epithelial cell apoptosis and inflammation via targeting miR-18a-5p/IGF1 axis.The reviews of this paper are available via the supplemental material section.

Optical linear frequency sweep based on a mode-spacing swept comb and multi-loop phase-locking for FMCW interferometry.

We report on the generation of a highly coherent broadband optical linear frequency sweep (LFS) using mode-spacing swept comb and multi-loop composite optical phase-locked loop (OPLL). We exploit a specially designed agile opto-electronic frequency comb as a sweeping reference, whose mode-spacing is capable of arbitrary frequency sweep while preserving a stable phase and power distribution per mode. By locking a continuous-wave (CW) laser to any of its modes using composite OPLL with a large loop bandwidth, it allows the extraction of the optical LFS at high-order modes in a coherent manner with a multiplied sweep range and rate. With such capability, only intermediate frequency LFS with smaller bandwidth is required to yield a broadband LFS while inheriting the coherence and precision from the comb. We achieve optical LFS of 60 GHz at 6 THz/s sweep rate with a nine-folded sweep bandwidth of the driving signal. Fourier transform-limited spatial resolution at more than 80 times of the intrinsic coherence length of the CW laser is demonstrated in an OFMCW interferometry, verifying the high coherence with more than 4 orders of magnitude improvement in spatial resolution. The characteristics in terms of agility, coherence, and precision are discussed together with the potential limitations. The proposed method is capable of generating arbitrary frequency-modulated optical waveforms with a multiplied bandwidth, showing attractive potential in future metrology applications.

LncRNA SNHG16 promotes pulmonary fibrosis by targeting miR-455-3p to regulate the Notch2 pathway.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung diseases with a poor prognosis. Long non-coding RNAs (lncRNAs) have been reported to be involved in IPF in several studies. However, the role of lncRNA SNHG16 in IPF is largely unknown. METHODS: Firstly, experimental pulmonary fibrosis model was established by using bleomycin (BML). Histology and Western blotting assays were used to determine the different stages of fibrosis and expression of several fibrosis biomarkers. The expression of SNHG16 was detected by quantitative real-time polymerase chain reaction (qRT-PCR). EdU staining and wound-healing assay were utilized to analyze proliferation and migration of lung fibroblast cells. Molecular mechanism of SNHG16 was explored by bioinformatics, dual-luciferase reporter assay, RNA immunoprecipitation assay (RIP), and qRT-PCR. RESULTS: The expression of SNHG16 was significantly up-regulated in bleomycin-(BLM) induced lung fibrosis and transforming growth factor-ß (TGF-ß)-induced fibroblast. Knockdown of SNHG16 could attenuate fibrogenesis. Mechanistically, SNHG16 was able to bind and regulate the expression of miR-455-3p. Moreover, SNHG16 also regulated the expression of Notch2 by targeting miR-455-3p. Finally, SNHG16 could promote fibrogenesis by regulating the expression of Notch2. CONCLUSION: Taken together, our study demonstrated that SNHG16 promoted pulmonary fibrosis by targeting miR-455-3p to regulate the Notch2 pathway. These findings might provide a novel insight into pathologic process of lung fibrosis and may provide prevention strategies in the future.