Additional file 6 of Trends in prevalence and incidence of chronic respiratory diseases from 1990 to 2017

Additional file 6: Figure S4. The correlation between the change of socio-demographic index (SDI) and the estimated annual percentage change (EAPC) in the age-standardized incidence rate (ASIR) of chronic obstructive pulmonary disease (COPD), pneumoconiosis, asthma and interstitial lung disease and pulmonary sarcoidosis from 1990 to 2017

Additional file 2 of Trends in prevalence and incidence of chronic respiratory diseases from 1990 to 2017

Additional file 2: Table S2. The global incidence, ASIR, prevalence and ASPR due to chronic respiratory diseases in 1990 and 2017

Additional file 5 of Trends in prevalence and incidence of chronic respiratory diseases from 1990 to 2017

Additional file 5: Figure S3. The correlation between socio-demographic index (SDI) and age-standardized incidence rate (ASIR) of chronic obstructive pulmonary disease (COPD), pneumoconiosis, asthma and interstitial lung disease and pulmonary sarcoidosis in 2017

Additional file 3 of Trends in prevalence and incidence of chronic respiratory diseases from 1990 to 2017

Additional file 3: Figure S1. The global incidence rate of chronic obstructive pulmonary disease (COPD), pneumoconiosis, asthma and interstitial lung disease and pulmonary sarcoidosis by age and sex in 1990

Additional file 4 of Trends in prevalence and incidence of chronic respiratory diseases from 1990 to 2017

Additional file 4: Figure S2. The age-standardized incidence rate (ASIR) of chronic obstructive pulmonary disease (COPD), pneumoconiosis, asthma and interstitial lung disease and pulmonary sarcoidosis in countires classified by the World Bank income levels during 1990–2017

Additional file 1 of Trends in prevalence and incidence of chronic respiratory diseases from 1990 to 2017

Additional file 1: Table S1. International Classification of Diseases and Injuries-10 (ICD-10) diagnosis code

Stable expression miR-127 affects senescence phenotypes in WI-38 fibroblasts.

<p>(A) Stable expression of miR-127 in WI-38 cells infected by lentiviral constructs and endogenous expression of miR-127 in senescent WI-38 cells were evaluated by qRT-PCR analysis. Data are presented as the mean ± SD from three independent experiments. (B) Growth curves of WI-38 cells stably infected with pLenti6/V5-D-premiR-127 or pLenti6/V5-D-YFP. Cells were counted every two days for two weeks. Data are presented as the mean ± SD from three independent experiments. (C) SA-β-gal staining of senescent cells induced by stable overexpression of miR-127. The WI-38 cells were stained for SA-β-gal activity 10 days after lentiviral infection. (D) Western blot analysis of senescence-associated proteins in WI-38 cells 6 days after lentiviral infection. β-actin was used for normalization.</p

miR-127 Regulates Cell Proliferation and Senescence by Targeting BCL6

<div><p>Cellular senescence occurs as a response to extracellular and intracellular stresses and contributes to aging and age-related pathologies. Emerging evidence suggests that cellular senescence also acts as a potent tumor suppression mechanism that prevents the oncogenic transformation of primary human cells. Recent reports have indicated that miRNAsact as key modulators of cellular senescence by targeting critical regulators of the senescence pathways. We previously reported that miR-127 is up-regulated in senescent fibroblasts. In this report, we identified miR-127 as a novel regulator of cellular senescence that directly targets BCL6. We further showed that miR-127 is down-regulated in breast cancer tissuesand that this down-regulation is associated with up-regulation of BCL6. Over-expression of miR-127 or depletion of BCL6 inhibits breast cancer cell proliferation. Our data suggest that miR-127 may function as a tumor suppressor that modulates the oncogene BCL6.</p></div

BCL6 is potentially involved in miR-127-mediated cellular senescence.

<p>(A–B) Growth curves of WI-38 and IMR-90 cells transiently transfected with 50 nM BCL6 siRNA or negative control. Growth curves were generated by cell number at indicated times. Data are presented as the mean ± SD from three-independent experiments. (C) SA-β-gal staining of senescent cells induced by transient transfection of BCL6 siRNA. The WI-38 and IMR-90 cells were stained 7 days after transfection with 50 nM BCL6 siRNA or negative control. (D) Western blot analysis of BCL6, cyclin D1, p53, and p21 in WI-38 and IMR-90 cells transiently transfected with 50 nM BCL6 siRNA or negative control. β-actin was used for normalization. (E) Western blot analysis of the expression of BCL6 in miR-127-expressing WI-38 cells transiently transfected with pcDNA3.0 and pcDNA3.0-BCL6. (F and G) Growth curve (F) and SA-β-gal activity (G) in miR-127-expressing WI-38 cells transfected by pcDNA3.0 and pcDNA3.0-BCL6. Cells were counted every two days for a week. The cells were stained SA-β-gal activity at 7 days after transfection with pcDNA3.0 or pcDNA3.0-BCL6. Data are presented as the mean ± SD from three independent experiments (*P<0.05, **P<0.01).</p

miR-127 is up-regulated in senescent human fibroblasts and mediates cellular senescence.

<p>(A) Relative levels of miR-127 expression analyzed by stem-loop qRT-PCR in different PDLs of WI-38 and IMR-90 cells. U6 RNA was used for normalization. Data are presented as the mean ± SD from three independent experiments. (B) Growth curves of WI-38 and IMR-90 cells transfected with 50 nM miR-127 mimic and negative control. Growth curves were generated by cell number at the indicated times. Data are presented as the mean ± SD from three independent experiments. (C) SA-β-gal staining of senescent cells induced by miR-127. The WI-38 and IMR-90 cellswere stained for SA-β-gal activity 7 days after transfection with 50 nM miR-127 mimic or negative control. (D) Western blot analysis of cyclin D1, p53, and p21 in WI-38 and IMR-90 cells at 72 hours post-transfection with the 50 nM miR-127-3p mimic or negative control. β-actin was used for normalization. (E) Cell cycle analysis was performed at 48 h after transfection. The histogram displays the percentage changes of G₀/G₁ and G₂/M when WI-38 cells transfected with miR-127 mimics and negative control. M1 and M2 show the spike of G₀/G₁ and G₂/M, respectively. Data are presented as the mean ± SD from three independent experiments (*P<0.05, **P<0.01).</p