Silicosis is a lung fibrotic disease caused by chronic silica exposure. Aberrations in long non-coding RNA (lncRNA) expression are associated with fibrotic diseases, but the role of lncRNAs in silicosis pathogenesis remains unclear. Here, we investigated the expression of lncRNAs during silicosis and the role of MRAK050699 in epithelial–mesenchymal transition (EMT). Differentially expressed lncRNAs in the lung tissues of normal and silicosis rats were compared, and their biological effects were determined using the Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. There were 1077 differentially expressed lncRNAs (378 upregulated and 699 downregulated). MRAK052509, MRAK139674, AY539881, MRAK050699, XR_6113, and BC167061 were selected to verify expression in silicosis rats using quantitative reverse transcription polymerase chain reaction. MRAK050699 was knocked down in rat alveolar type II epithelial cells, and the molecular mechanism of transforming growth factor-β (TGF-β)-induced EMT in these cells was studied. All selected lncRNAs were upregulated in the silicosis rats, consistent with the sequencing results. MRAK050699 knockdown inhibited EMT of RLE-6TN cells by regulating the TGF-β/Smad3 signaling pathway. Thus, the differential expression of lncRNAs is related to silicosis development, and MRAK050699 plays an important role in EMT, suggesting a potential therapeutic target for silicosis.
Our aim was to clarify the main factors associated with lung function and to analyze the correlation between fine particulate matter (PM 2.5 ) and lung function in a rural Chinese population. We analyzed data of 5195 participants in the China Northwest Natural Population Cohort: Ningxia Project who were ≥ 30 years old. They were recruited from 2018 to 2019, underwent spirometry during the physical examination, and completed a self-report questionnaire. A satellite-based spatiotemporal model was used to estimate the 2-year average PM 2.5 exposure based on participants' home addresses. A generalized linear mixed model was used to test the relationship between PM 2.5 concentration and lung function. Sex, age, exposure to cooking oil fumes, and occupational exposure were negatively correlated (P < 0.05) with forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV 1 ). Educational status, economic level, tea consumption, and alcohol consumption were positively correlated (P < 0.05) with FVC and FEV 1 . The adjusted results of each model revealed that FVC and FEV 1 decreased with increased exposure to PM 2.5 . There was a strong negative correlation between a PM 2.5 concentration of 35.66 μg/m 3 and FVC, FEV1, and FEV1/FVC, with unadjusted hazard ratios of − 0.06 (95% confidence interval, − 0.10 to − 0.01), − 0.13 (− 0.17 to − 0.10), and − 22.10 (− 24.62 to − 19.26), respectively. In conclusion, long-term exposure to high concentrations of ambient PM 2.5 is related to reduce lung function among people in rural areas in northwestern China.
Background In recent decades, obesity has become an epidemic worldwide and is a risk factor for many chronic diseases. Lung function is also a predictor of various chronic diseases. However, research results on the association between obesity and lung function are inconsistent and few studies have evaluated the association between central obesity indicators and lung function. Therefore, this study explored the correlation between central obesity and lung function. Methods This study is a cross-sectional study. The basic participant characteristics were collected by questionnaire. A tape measure was used to measure waist circumference (WC) and hip circumference (HC). Body fat percentage was measured using an InBody370. Lung function parameters were measured using a digital spirometer connected to a computer (Chestgraph HI-101). R (R4.0.5) software was used for data analysis. A generalized linear model was used to analyze the association between obesity and lung function. Results This study found that body mass index (BMI) adjusted for WC was negatively correlated with forced vital capacity (FVC) (β=−0.05 [−0.06, −0.03] in men, β=−0.05 [−0.07, −0.04] in women) and forced expiratory volume in 1 s (FEV1)(β=−0.02 [−0.03, −0.00] in men, β=−0.03 [−0.04, −0.02] in women). Body fat percentage was negatively correlated with FVC (β=−0.01 [−0.01, −0.01] in men, β=−0.01 [−0.01, −0.00] in women). Conclusion Central obesity and combined central and general obesity were more strongly positively correlated with lung function. WC-adjusted BMI was negatively correlated with lung function. Body fat percentage was negatively correlated with lung function.
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