| Summary: | Objective To explore the effect and preliminary mechanism of stathmin on skin fibroblast migration in the early inflammatory reaction of wound healing mimicked by TNF-α stimulation. Methods Human dermal fibroblast was stimulated by TNF-α to establish a cell model of inflammation at the early stage of wound healing. The effect of TNF-α on filopodium formation was observed by immunofluorescence assay, cell migration was detected by scratch wound healing, and stathmin expression level under TNF-α stimulation was measured by immunofluorescence assay and Western blotting. After cytochalasin B stimulation and small interfering RNA were used to interfere stathmin expression, respectively, immunofluorescence assay and scratch wound healing were performed again to observe the changes of filopodia and cell migration. Results TNF-α treatment promoted the formation of filopodia in human dermal fibroblasts, enhanced cell migration (P < 0.05) and increased stathmin expression (P < 0.05). Cytochalasin B treatment reduced the formation of filopodia and cell migration (P < 0.05); and interference of stathmin expression suppressed the formation of filopodia and reduced cell migration (P < 0.05). Conclusion In early inflammation, stathmin mediates skin fibroblast migration by promoting the formation of filopodia.
|
|---|