Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
[Cytochalasin B-Induced adipose stem cell-derived nanovesicles promote hair follicle regeneration via activation of the β-catenin signaling pathway].
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Wang Lei, Liu Yiwen, Cai Peiyun, Mao Xuerui, Tian Tian, Cao Lei
Аннотация
OBJECTIVES: To evaluate the regulatory effects of adipose stem cell (ADSC)-derived cytochalasin B-induced nanovesicles (CINVs) on the biological functions of dermal papilla cells (DPCs) and on hair follicle cycle transition, and to explore the underlying molecular mechanisms.
METHODS: CINVs were prepared from ADSCs. Their effects on DPC proliferation, migration, and apoptosis were assessed in vitro. A mouse depilation model was used to evaluate the ability of CINVs to promote the transition of hair follicles from telogen to anagen. Western blotting, hematoxylin-eosin (HE) staining, and immunofluo-rescence analyses were performed to assess the activation of β-catenin-related signaling pathways and to elucidate the molecular mechanisms of CINV-mediated hair follicle regeneration.
RESULTS: CCK-8 assays showed that CINVs at 40 and 60 μg/mL significantly enhanced DPC proliferation. Wound healing assays (at 40 μg/mL) confirmed that CINVs markedly promoted DPC migration. Western blotting revealed that, compared with the control group, CINV treatment significantly increased the expression of phosphorylated GSK-3β (p-GSK-3β, P<0.05) and upregulated β-catenin, the core effector of the canonical Wnt/β-catenin pathway (P<0.01). Moreover, cyclin D1 (a positive regulator of cell cycle progression) expression was elevated (P<0.05), and the levels of phosphorylated AKT (p-AKT, associated with cell survival) and phosphorylated ERK (p-ERK, associated with cell proliferation) were significantly increased (both P<0.05). The Bcl-2/Bax ratio (an anti-apoptotic index) was also increased. In vivo, CINV-treated mice displayed darkened dorsal skin and enlarged hair bulb diameters, along with elevated proportions of β-catenin- and Ki67-positive cells. These effects were significantly attenuated by co-administration of the β-catenin inhibitor MSAB.
CONCLUSIONS: ADSC-derived CINVs effectively regulate the biological functions of DPCs and promote the transition of hair follicles from telogen to anagen, primarily through activation of the β-catenin signaling pathway.
METHODS: CINVs were prepared from ADSCs. Their effects on DPC proliferation, migration, and apoptosis were assessed in vitro. A mouse depilation model was used to evaluate the ability of CINVs to promote the transition of hair follicles from telogen to anagen. Western blotting, hematoxylin-eosin (HE) staining, and immunofluo-rescence analyses were performed to assess the activation of β-catenin-related signaling pathways and to elucidate the molecular mechanisms of CINV-mediated hair follicle regeneration.
RESULTS: CCK-8 assays showed that CINVs at 40 and 60 μg/mL significantly enhanced DPC proliferation. Wound healing assays (at 40 μg/mL) confirmed that CINVs markedly promoted DPC migration. Western blotting revealed that, compared with the control group, CINV treatment significantly increased the expression of phosphorylated GSK-3β (p-GSK-3β, P<0.05) and upregulated β-catenin, the core effector of the canonical Wnt/β-catenin pathway (P<0.01). Moreover, cyclin D1 (a positive regulator of cell cycle progression) expression was elevated (P<0.05), and the levels of phosphorylated AKT (p-AKT, associated with cell survival) and phosphorylated ERK (p-ERK, associated with cell proliferation) were significantly increased (both P<0.05). The Bcl-2/Bax ratio (an anti-apoptotic index) was also increased. In vivo, CINV-treated mice displayed darkened dorsal skin and enlarged hair bulb diameters, along with elevated proportions of β-catenin- and Ki67-positive cells. These effects were significantly attenuated by co-administration of the β-catenin inhibitor MSAB.
CONCLUSIONS: ADSC-derived CINVs effectively regulate the biological functions of DPCs and promote the transition of hair follicles from telogen to anagen, primarily through activation of the β-catenin signaling pathway.