Dong Zhu-Ge1, Yu-Ping Yang1, Zi-Jun Jiang2. 1. Department of General Medicine, East Medical District of Linyi People's Hospital, Linyi 276000, Shandong, China. 2. Emergency Department, East Medical District of Linyi People's Hospital, Linyi 276000, Shandong, China. Electronic address: iodine.bqa99289@gmail.com.
Abstract
OBJECTIVE: Pneumonia is the leading global cause of mortality and morbidity in children and elderly people worldwide. The lncRNA colorectal neoplasia differentially expressed (CRNDE) plays an important role in the human development and disease progression. The present study was aimed to investigate the effect of CRNDE on LPS-induced injuries in WI-38 cells and explore the potential mechanism. METHODS: WI-38 cells were treated with LPS to induce injuries. The expression of CRNDE and FOXM1 in WI-38 cells were altered by transient transfection assay. Cell viability was measured by CCK-8 assay and cell apoptosis was detected by flow cytometry assay and western blot. The levels of inflammatory cytokines were assessed by ELISA and western blot. Furthermore, western blot analysis was performed to detect the expression levels of NF-κB and JAK/STAT pathway-related proteins. RESULTS: LPS exposure induced cell injuries and increased CRNDE expression in WI-38 cells. CRNDE overexpression enhanced cell injuries in WI-38 cells with significantly reducing cell viability, increasing cell apoptosis and inflammatory cytokines levels. In addition, CRNDE overexpression further activated the NF-κB and JAK/STAT pathways in LPS-injured WI-38 cells. Inversely, opposite results were observed in CRNDE inhibition treatment group. Interestingly, FOXM1 was up-regulated by CRNDE and FOXM1 silence blocked the effect of CRNDE overexpression in cell apoptosis, inflammation and activation of NF-κB and JAK/STAT signaling pathways. CONCLUSION: This study demonstrated that CRNDE overexpression accelerated LPS-induced apoptosis and inflammation via up-regulation of FOXM1 in WI-38 cells.
OBJECTIVE: Pneumonia is the leading global cause of mortality and morbidity in children and elderly people worldwide. The lncRNA colorectal neoplasia differentially expressed (CRNDE) plays an important role in the human development and disease progression. The present study was aimed to investigate the effect of CRNDE on LPS-induced injuries in WI-38 cells and explore the potential mechanism. METHODS: WI-38 cells were treated with LPS to induce injuries. The expression of CRNDE and FOXM1 in WI-38 cells were altered by transient transfection assay. Cell viability was measured by CCK-8 assay and cell apoptosis was detected by flow cytometry assay and western blot. The levels of inflammatory cytokines were assessed by ELISA and western blot. Furthermore, western blot analysis was performed to detect the expression levels of NF-κB and JAK/STAT pathway-related proteins. RESULTS:LPS exposure induced cell injuries and increased CRNDE expression in WI-38 cells. CRNDE overexpression enhanced cell injuries in WI-38 cells with significantly reducing cell viability, increasing cell apoptosis and inflammatory cytokines levels. In addition, CRNDE overexpression further activated the NF-κB and JAK/STAT pathways in LPS-injured WI-38 cells. Inversely, opposite results were observed in CRNDE inhibition treatment group. Interestingly, FOXM1 was up-regulated by CRNDE and FOXM1 silence blocked the effect of CRNDE overexpression in cell apoptosis, inflammation and activation of NF-κB and JAK/STAT signaling pathways. CONCLUSION: This study demonstrated that CRNDE overexpression accelerated LPS-induced apoptosis and inflammation via up-regulation of FOXM1 in WI-38 cells.