Eun Byul Cho1, Gil Soon Park2, Seok Soon Park3, Ye Ji Jang1, Kwang Ho Kim1, Kwang Joong Kim1, Eun Joo Park1. 1. Department of Dermatology, College of Medicine, Hallym University, Anyang, Korea. 2. Department of Dermatology, Hallym Institute for Translational medicine, Anyang, Korea. 3. Asan Institute for Life Sciences, Department of Convergence Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Abstract
BACKGROUND: Platelet-rich plasma (PRP) is a blood fraction that contains high concentrations of several growth factors. PRP has been recently used in skin wound healing and rejuvenation. However, the precise molecular mechanisms underlying PRP-induced wound healing are unknown. AIMS: This study aimed to evaluate the effects of PRP on extracellular matrix remodeling, which requires the activation of dermal fibroblasts. METHODS: Cell proliferation and migration assay, enzyme-linked immunosorbent analysis, and Western blotting were performed on PRP-treated human skin fibroblasts. RESULTS: Platelet numbers were enhanced by 4.6-fold in PRP compared to that in whole blood. PRP stimulated the proliferation and migration of human dermal fibroblasts and increased the expression of human procollagen I alpha 1, elastin, MMP-1, and MMP-2 in human dermal fibroblasts. PRP-treated human dermal fibroblasts also showed a dramatic reduction in the phosphorylation of c-Jun N-terminal kinase (JNK), whereas total JNK levels were not significantly reduced. CONCLUSIONS: Collectively, PRP induced increased expression of type I collagen, elastin, MMP-1, and MMP-2, thereby accelerating wound healing. Our findings reveal basic mechanisms underlying PRP-mediated tissue remodeling. Thus, these results could be exploited for clinical dermatology and skin rejuvenation.
BACKGROUND: Platelet-rich plasma (PRP) is a blood fraction that contains high concentrations of several growth factors. PRP has been recently used in skin wound healing and rejuvenation. However, the precise molecular mechanisms underlying PRP-induced wound healing are unknown. AIMS: This study aimed to evaluate the effects of PRP on extracellular matrix remodeling, which requires the activation of dermal fibroblasts. METHODS: Cell proliferation and migration assay, enzyme-linked immunosorbent analysis, and Western blotting were performed on PRP-treated human skin fibroblasts. RESULTS: Platelet numbers were enhanced by 4.6-fold in PRP compared to that in whole blood. PRP stimulated the proliferation and migration of human dermal fibroblasts and increased the expression of human procollagen I alpha 1, elastin, MMP-1, and MMP-2 in human dermal fibroblasts. PRP-treated human dermal fibroblasts also showed a dramatic reduction in the phosphorylation of c-Jun N-terminal kinase (JNK), whereas total JNK levels were not significantly reduced. CONCLUSIONS: Collectively, PRP induced increased expression of type I collagen, elastin, MMP-1, and MMP-2, thereby accelerating wound healing. Our findings reveal basic mechanisms underlying PRP-mediated tissue remodeling. Thus, these results could be exploited for clinical dermatology and skin rejuvenation.
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