Study summary · research use only
Cathelicidin LL-37 promotes wound healing in diabetic mice by regulating TFEB-dependent autophagy
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study used a diabetic mouse model of full-thickness wound closure, along with in vitro HaCat keratinocyte experiments, to examine whether the human cathelicidin LL-37 affects wound healing through autophagy. The abstract reports LL-37 treatment was associated with improved wound healing in diabetic mice, an effect reversed by the autophagy inhibitor 3-MA. In high-glucose conditions in vitro, 3-MA reduced LL-37's effect on promoting HaCat keratinocyte migration. LL-37 promoted nuclear translocation of transcription factor EB (TFEB) and increased expression of ATG5, ATG7, and beclin 1 (BECN1), changes blocked by TFEB knockdown, which also reduced LL-37's effect on keratinocyte migration. The authors describe these findings as linking LL-37 to TFEB-dependent autophagy in diabetic wound healing.
Abstract
Diabetic patients often experience impaired wound healing. Human cathelicidin LL-37 possesses various biological functions, such as anti-microbial, anti-inflammatory, and pro-wound healing activities. Autophagy has important effects on skin wound healing. However, little is known about whether LL-37 accelerates diabetic wound healing by regulating autophagy. In the study, we aimed to investigate the role of autophagy in LL-37-induced wound healing and uncover the underlying mechanisms involved. A full-thickness wound closure model was established in diabetic mice to evaluate the effects of LL-37 and an autophagy inhibitor (3-MA) on wound healing. The roles of LL-37 and 3-MA in regulating keratinocyte migration were assessed using transwell migration and wound healing assays. The activation of transcription factor EB (TFEB) was measured using western blotting and immunofluorescence (IF) assays of its nuclear translocation. The results showed that LL-37 treatment improved wound healing in diabetic mice, whereas these effects were reversed by 3-MA. In vitro, 3-MA decreased the effects of LL-37 on promoting HaCat keratinocyte migration in the presence of high glucose (HG). Mechanistically, LL-37 promoted TFEB activation and resulted in subsequent activation of autophagy, as evidenced by increased nuclear translocation of TFEB and increased expression of ATG5, ATG7, and beclin 1 (BECN1), whereas these changes were blocked by TFEB knockdown. As expected, TFEB knockdown damaged the effects of LL-37 on promoting keratinocyte migration. Collectively, these results suggest that LL-37 accelerates wound healing in diabetic mice by activating TFEB-dependent autophagy, providing new insights into the mechanism by which LL-37 promotes diabetic wound healing.
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