Endothelial dysfunction is associated with the progression of
sepsis. This study sought to probe the molecular route of sex-determining region on the Y chromosome-box
transcription factor 18 (SOX18) in
sepsis-associated endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with
lipopolysaccharide (LPS) to establish the
sepsis cell model. Cell viability,
lactate dehydrogenase (LDH) release, oxidative stress (
reactive oxygen species/
malondialdehyde/
superoxide dismutase), and
inflammation (
interleukin-1β/
tumor necrosis factor-α/
interleukin-6) were evaluated by cell counting kit-8 assay and relevant assay kits. The expression levels of SOX18,
microRNA (miR)-204-5p, and
cadherin-2 (CDH2) in cells were determined by real-time quantitative polymerase chain reaction and Western blot assay. The interaction of SOX18, miR-204-5p, and CDH2 was analyzed by
chromatin immunoprecipitation and dual-
luciferase assay. LPS induced HUVECs injury and downregulation of SOX18. SOX18 overexpression increased cell viability, while decreased LDH activity, oxidative stress, and
inflammation. SOX18 bound to the miR-204-5p promoter to promote miR-204-5p expression, and further repressed CDH2 expression. miR-204-5p knockdown and CDH2 overexpression abrogated the protective role of SOX18 in HUVECs injury. Overall, SOX18 alleviated LPS-induced injury of HUVECs by promoting miR-204-5p and repressing CDH2, suggesting it as a potential target for
sepsis treatment.