Wnt/β-catenin signaling activator restores hair regeneration suppressed by diabetes mellitus
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Diabetes mellitus is one of the most prevalent diseases inmodern society. Many complicationssuch as hepatic cirrhosis,neuropathy, cardiac infarction, and so on are associated withdiabetes. Although a relationship between diabetes and hairloss has been recently reported, the treatment of diabetic hairloss by Wnt/β-catenin activators has not been achieved yet. Inthis study, we found that the depilation-induced anagen phasewas delayed in both db/db mice and high-fat diet (HFD) andstreptozotocin (STZ)-induced diabetic mice. In diabetic mice,both hair regrowth and wound-induced hair follicle neogenesis(WIHN) were reduced because of suppression of Wnt/β-catenin signaling and decreased proliferation of hair folliclecells. We identified that KY19382, a small molecule that activatesWnt/β-catenin signaling, restored the capabilities of regrowthand WIHN in diabetic mice. The Wnt/β-catenin signalingactivator also increased the length of the human hair folliclewhich was decreased under high glucose culture conditions. Overall, the diabetic condition reduced both hair regrowthand regeneration with suppression of the Wnt/β-catenin signalingpathway. Consequently, the usage of Wnt/β-catenin signalingactivators could be a potential strategy to treat diabetes-inducedalopecia patients.
Abstract
Diabetes mellitus is one of the most prevalent diseases inmodern society. Many complicationssuch as hepatic cirrhosis,neuropathy, cardiac infarction, and so on are associated withdiabetes. Although a relationship between diabetes and hairloss has been recently reported, the treatment of diabetic hairloss by Wnt/β-catenin activators has not been achieved yet. Inthis study, we found that the depilation-induced anagen phasewas delayed in both db/db mice and high-fat diet (HFD) andstreptozotocin (STZ)-induced diabetic mice. In diabetic mice,both hair regrowth and wound-induced hair follicle neogenesis(WIHN) were reduced because of suppression of Wnt/β-catenin signaling and decreased proliferation of hair folliclecells. We identified that KY19382, a small molecule that activatesWnt/β-catenin signaling, restored the capabilities of regrowthand WIHN in diabetic mice. The Wnt/β-catenin signalingactivator also increased the length of the human hair folliclewhich was decreased under high glucose culture conditions. Overall, the diabetic condition reduced both hair regrowthand regeneration with suppression of the Wnt/β-catenin signalingpathway. Consequently, the usage of Wnt/β-catenin signalingactivators could be a potential strategy to treat diabetes-inducedalopecia patients.
참고문헌 (38)
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