Conclusions
BATF knockdown alleviated NS-induced lung injury by activating the MAPK/NF-κB pathway via transcriptionally upregulating COTL1 expression.
Material and methods
An in vivo model of NS was established using cecal slurry (CS). H&E staining was applied for observing the severity of lung injury in tissues of mice. MTT assay was applied for determining cell viability, and the inflammatory factors were examined using ELISA. Apoptosis was assessed via flow cytometry. Superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) levels were assessed by commercial kits. The interaction between basic leucine zipper ATF-like transcription factor (BATF) and COTL1 was verified using dual luciferase reporter and chromatin immunoprecipitation (ChIP) assay.
Methods
An in vivo model of NS was established using cecal slurry (CS). H&E staining was applied for observing the severity of lung injury in tissues of mice. MTT assay was applied for determining cell viability, and the inflammatory factors were examined using ELISA. Apoptosis was assessed via flow cytometry. Superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) levels were assessed by commercial kits. The interaction between basic leucine zipper ATF-like transcription factor (BATF) and COTL1 was verified using dual luciferase reporter and chromatin immunoprecipitation (ChIP) assay.
Results
COTL1 knockdown alleviated the progression of NS-induced lung injury. COTL1 knockdown enhanced the viability and decreased interleukin (IL)-6 and IL-1 β levels in lipopolysaccharides (LPS)-stimulated pulmonary microvascular endothelial cells. Silencing of COTL1 inhibited LPS induced apoptosis and oxidative stress. More importantly, BATF activated MAPK/NF-κB signaling through transcriptionally upregulating COTL1. Furthermore, BATF improved the LPS-induced inflammatory response and apoptosis in pulmonary microvascular endothelial cells through mediation of COTL1. Conclusions: BATF knockdown alleviated NS-induced lung injury by activating the MAPK/NF-κB pathway via transcriptionally upregulating COTL1 expression.