Table 2.

Studies dealing with bronchial hypersensitivity (avSG: antiviral stress granules; COPD: chronic obstructive pulmonary disease; pBECs: primary bronchial epithelial cells; PH: pulmonary hypertension; PKR: protein kinase R; PTEN: phosphatase and tensin homolog; SAECs: small airway epithelial cells).

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)