Table 2.
Bronchial Hypersensitivity | ||||
---|---|---|---|---|
Humans | ||||
Study | Disease | Sample | miRNAs | Findings |
Baker et al. (2016) [37] | COPD | Peripheral lung samples from COPD patients and controls; airway epithelial cells | miR-34a | miR-34a antagomirs increased SIRT1 (p < 0.01)/-6 (p < 0.05) mRNA levels, decreasing cellular senescence markers in COPD (p < 0.05) |
Hsu et al. (2016) [76] | COPD | Five COPD, five smokers, five controls | miR-132 | Ectopic expression of PKR or miR-132 antagomiR alone failed to restore IFN-β induction (p > 0.05), co-treatment increased avSG formation, induction of p300, and IFN-β in COPD pBECs (p < 0.05) |
Jiang et al. (2018) [49] | COPD | Humans: 73 patients with PH, 32 controls. Animals: hypoxia-induced PH mice |
miR-190a-5p | Antagomir-190a-5p reduced right ventricular systolic pressure (p < 0.01) and enhanced KLF15 expression (p < 0.0001) in lung tissue |
Baker et al. (2019) [38] | COPD | 30 COPD/18 controls: lung tissue from tissue bank; 14 COPD, 10 non-smoking controls: human primary SAECs cultured; 13 COPD, five controls: sputum samples collected | miR-570-3p | Inhibition of elevated miR-570-3p in COPD small airway epithelial cells, using an antagomir, restores sirtuin-1, and suppresses markers of cellular senescence, restoring cellular growth (p < 0.05) |
Animals | ||||
Study | Disease | Sample | miRNAs | Findings |
Collison et al. (2011) [24] | Allergic airway disease | BALB/c mice sensitized with house dust mite | miR-145, miR-21, let-7b | Inhibition of miR-145 (p < 0.05), but not miR-21 or let-7b (both p > 0.05), inhibited eosinophilic inflammation, mucus hypersecretion, TH2 cytokine production, and airway hyper-responsiveness |
Li et al. (2015) [50] | Airway hyper-responsiveness | Wild-type specific pathogen-free BALB/c mice | miR-9 | AntagomiR-9 increased PP2A activity and GR nuclear translocation in macrophages (p < 0.05), restored steroid sensitivity in steroid-resistant airway hyper-responsiveness |
Plank et al. (2015) [30] | Asthma | Specific pathogen-free BALB/c mice | miR-155-5p | Antagomir administration reduced miR-155-5p expression (p < 0.01), but failed to alter the disease phenotype (p > 0.05). It exhibits poor uptake in lymphocytes |
Kim et al. (2017) [27] | Asthma | BALB/c mice | miR-21 | Antagomir-21 increased PTEN levels (p < 0.05). Treatment with Ant-21 reduced PI3K activity and restored HDAC2 levels (p < 0.05), suppressing airway hyper-responsiveness and restoring steroid sensitivity to allergic airway disease |
Lee et al. (2017) [35] | Acute bronchial asthma | BALB/c mice sensitized and challenged with ovalbumin | miR-21 | MiR-21 expression down-regulated in mice lungs treated with anti-miR-21. It reduced total cell (p < 0.001) and eosinophil counts (p < 0.01) in BAL fluid and the levels of IL-5 and IL-13 (p < 0.05) |
Jiang et al. (2018) [49] | COPD | Humans: 73 patients with PH, 32 controls. Animals: hypoxia-induced PH mice |
miR-190a-5p | Antagomir-190a-5p reduced right ventricular systolic pressure (p < 0.01) and enhanced the KLF15 expression levels (p < 0.0001) in lung tissue |
Cell Lines | ||||
Study | Disease | Sample | miRNAs | Findings |
Baker et al. (2016) [37] | COPD | Peripheral lung samples from COPD patients and controls; airway epithelial cells | miR-34a | miR-34a antagomirs increased SIRT1 (p < 0.01)/-6 (p < 0.05) mRNA levels, decreasing markers of cellular senescence in airway epithelial cells from COPD (p < 0.05) |
Hsu et al. (2016) [76] | COPD | Five COPD, five smokers, five controls | miR-132 | Ectopic expression of PKR or miR-132 antagomiR alone failed to restore IFN-β induction (p > 0.05), co-treatment increased avSG formation, induction of p300 and IFN-β in COPD pBECs (p < 0.05) |
Baker et al. (2019) [38] | COPD | 30 COPD/18 controls: lung tissue from a tissue bank; 14 COPD, 10 non-smoking controls: human primary SAECs cultured; 13 COPD, five controls: sputum samples collected | miR-570-3p | Inhibition of elevated miR-570-3p in COPD small airway epithelial cells, using an antagomir, restores sirtuin-1 and suppresses markers of cellular senescence, restoring cellular growth (p < 0.05) |