Lasers in surgery and medicine · 2026
LLLT-ADSCs Curtail the Progression of Keloid Through Exosomal miR-26a-5p Downregulating Jag/Notch Pathway.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Han Bing, Yang Jifan, Bai Peiwen, Jiao Hu, Yuan Xiang, Shi Jun, Zhu Zhaowei, Su Zhicheng
Аннотация
BACKGROUND: Adipose-derived stem cells treated with low-level laser light (LLLT-ADSCs) demonstrate an inhibitory effect on keloid scars, although the underlying molecular mechanisms remain largely unknown. This study aims to elucidate these mechanisms.
METHODS: We investigated the morphology, quantity, and microRNA (miRNA) expression profiles of exosomes derived from LLLT-ADSCs compared to those from untreated ADSCs. Notably, hsa-miR-26a-5p was found to be highly expressed in exosomes from LLLT-ADSCs. We examined its impact on the proliferation, migration, and invasion of keloid fibroblasts (KFs) by modulating its expression levels in these cells. A dual-luciferase reporter assay was utilized to confirm the interaction between hsa-miR-26a-5p and the Jagged-1/Notch signaling pathway.
RESULTS: Significant variations were observed in the exosomal contents between LLLT-ADSCs and ADSCs. Enhanced expression of hsa-miR-26a-5p was associated with reduced proliferation, migration, and invasion of KFs, along with diminished expression of Jagged-1 and NICD proteins. Conversely, suppression of hsa-miR-26a-5p expression reversed these effects. The dual-luciferase reporter system demonstrated that modifications in the binding sites of Jag-1 significantly mitigated the downregulation of Jag-1 expression induced by miRNA interaction.
CONCLUSIONS: LLLT-ADSCs can produce and deliver hsa-miR-26a-5p via exosomes to suppress the Jagged-1/Notch pathway activation in KFs, thereby effectively preventing the progression of keloid scars. This mechanism presents a novel therapeutic strategy for managing keloid scars.
METHODS: We investigated the morphology, quantity, and microRNA (miRNA) expression profiles of exosomes derived from LLLT-ADSCs compared to those from untreated ADSCs. Notably, hsa-miR-26a-5p was found to be highly expressed in exosomes from LLLT-ADSCs. We examined its impact on the proliferation, migration, and invasion of keloid fibroblasts (KFs) by modulating its expression levels in these cells. A dual-luciferase reporter assay was utilized to confirm the interaction between hsa-miR-26a-5p and the Jagged-1/Notch signaling pathway.
RESULTS: Significant variations were observed in the exosomal contents between LLLT-ADSCs and ADSCs. Enhanced expression of hsa-miR-26a-5p was associated with reduced proliferation, migration, and invasion of KFs, along with diminished expression of Jagged-1 and NICD proteins. Conversely, suppression of hsa-miR-26a-5p expression reversed these effects. The dual-luciferase reporter system demonstrated that modifications in the binding sites of Jag-1 significantly mitigated the downregulation of Jag-1 expression induced by miRNA interaction.
CONCLUSIONS: LLLT-ADSCs can produce and deliver hsa-miR-26a-5p via exosomes to suppress the Jagged-1/Notch pathway activation in KFs, thereby effectively preventing the progression of keloid scars. This mechanism presents a novel therapeutic strategy for managing keloid scars.