Long non-coding RNA H19 deficiency ameliorates bleomycin-induced pulmonary inflammation and fibrosis [post]

XIAOYU WAN, XINBEI TIAN, JUN DU, YING LU, YONGTAO XIAO
2020 unpublished
Background: The poor understanding of pathogenesis in idiopathic pulmonary fibrosis (IPF) impaired development of effective therapeutic strategies. The aim of the current study is to investigate the roles of long non-coding RNA H19 (lncRNA H19) in the pathogenesis of IPF. Methods: Bleomycin was used to induce pulmonary inflammation and fibrosis in mice. The mRNAs and proteins expression in lung tissues was determined by quantitative real-time polymerase chain reaction and western blot. H19
more » ... tern blot. H19 knockout (H19-/-) mice were generated by CRISPR/Cas9 and used to investigate the roles of H19 in the pulmonary inflammation and fibrosis in vivo.Results: The expression of H19 mRNA was up-regulated in fibrotic lungs patients with IPF as well as in lungs tissues that obtained from bleomycin-treated mice. H19-/- mice suppressed bleomycin-mediated pulmonary inflammation and inhibited the Il6/Stat3 signaling. H19 deficiency ameliorated bleomycin-induced pulmonary fibrosis and repressed the activation of TGF-β/Smad and S1pr2/Sphk2 in the lungs of bleomycin-treated mice. Conclusions: Our data suggests that H19 is a profibrotic lncRNA and a potential therapeutic target for pulmonary fibrosis.
doi:10.21203/rs.3.rs-41983/v3 fatcat:5pxngj5banbppoxmq6ao5pqxgy