BACKGROUND: Acute lung injury is a life-threatening inflammatory lung condition. Studies have explored the role of lncRNA H19 in several diseases, including cancers. In this study, We aimed to explore the role of H19 in lipopolysaccharide (LPS)-induced lung injury and to elucidate the underlying molecular mechanism. METHODS: MRC-5 cells (lung fibroblast cells) were used in the experiment. Cell viability, proliferation, and apoptosis were measured by specific assays. qRT PCR and western blot estimated specific mRNAs and proteins, respectively. Short-hairpin RNA directed against human lncRNA H19 was ligated into plasmid and referred to as (sh-H19). Aagin, full-length Runx2 sequences and short-hairpin RNA directed against Runx2 were constructed in pEX-2 and plasmids respectively, and were referred as to pEX-Runx2 and sh-Runx2 Results: LPS significantly suppressed cell viability (P < 0.05) and migration (P < 0.01), and increased apoptosis (P < 0.001). LPS also significantly increased (p < 0.01) expression of H19. Suppression of H19 expression led to significant decrease in cell viability, migration and significant increase in apoptosis (P < 0.05). Although suppression of H19 was deleterious to cells, suppression of both miR181a and H19 led to opposite changes. Knockdown of miR-181a led to upregulation of Runx2 expression, which significantly improved (P < 0.05) cell viability, migration, and suppressed (P < 0.05) apoptosis. Overexpression of Runx2 also activated Notch and JNK pathways. CONCLUSION: H19 protected MRC-5 cells against LPS mediated cell injury by suppressing miR181 expression which in turn acts via promotion of Runx2 expression. Again, overexpression of Runx2 led to activation of Notch and JNK pathways. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
BACKGROUND: Acute lung injury is a life-threatening inflammatory lung condition. Studies have explored the role of lncRNA H19 in several diseases, including cancers. In this study, We aimed to explore the role of H19 in lipopolysaccharide (LPS)-induced lung injury and to elucidate the underlying molecular mechanism. METHODS: MRC-5 cells (lung fibroblast cells) were used in the experiment. Cell viability, proliferation, and apoptosis were measured by specific assays. qRT PCR and western blot estimated specific mRNAs and proteins, respectively. Short-hairpin RNA directed against human lncRNA H19 was ligated into plasmid and referred to as (sh-H19). Aagin, full-length Runx2 sequences and short-hairpin RNA directed against Runx2 were constructed in pEX-2 and plasmids respectively, and were referred as to pEX-Runx2 and sh-Runx2 Results: LPS significantly suppressed cell viability (P < 0.05) and migration (P < 0.01), and increased apoptosis (P < 0.001). LPS also significantly increased (p < 0.01) expression of H19. Suppression of H19 expression led to significant decrease in cell viability, migration and significant increase in apoptosis (P < 0.05). Although suppression of H19 was deleterious to cells, suppression of both miR181a and H19 led to opposite changes. Knockdown of miR-181a led to upregulation of Runx2 expression, which significantly improved (P < 0.05) cell viability, migration, and suppressed (P < 0.05) apoptosis. Overexpression of Runx2 also activated Notch and JNK pathways. CONCLUSION:H19 protected MRC-5 cells against LPS mediated cell injury by suppressing miR181 expression which in turn acts via promotion of Runx2 expression. Again, overexpression of Runx2 led to activation of Notch and JNK pathways. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.