Platelet-rich plasma (PRP) has been found effective in wound healing, yet the underlying mechanisms in the healing of diabetic wounds remain unclear. In this study, we focus on investigating the role of PRP in enhancing the wound healing in a diabetic mouse model, specially through the modulation of the PI3K/AKT signaling pathway and its effect on collagen production and angiogenesis in the wounds of diabetic mouse model. In our in vitro experiments, we observed that PRP, in a concentration-dependent manner, significantly stimulated the proliferation, migration, and collagen synthesis in human dermal fibroblasts. Concurrently, PRP activated the PI3K/AKT and TGF-β/SMAD2 signaling pathways. In vivo, utilizing a diabetic mouse model of wound healing, PRP treatment significantly enhanced wound healing by accelerating wound closure, improving collagen deposition and organization, and promoting angiogenesis, as evidenced by increased expression of CD31 and VEGF. Importantly, the application of the PI3K inhibitor LY294002 effectively inhibited the observed effects of PRP. Additionally, the activation of the TGF-β/SMAD2 signaling pathway induced by PRP was also suppressed when PI3K was inhibited, suggesting that the PI3K/AKT pathway functions upstream to regulate TGF-β/SMAD2 signaling. These findings elucidate the role of PRP in facilitating diabetic wound healing through the activation of the PI3K/AKT pathway, which subsequently cross-regulates TGF-β/SMAD2 signaling, thereby enhancing cellular functions vital for tissue regeneration. Our results contribute valuable mechanistic insights into the therapeutic potential of PRP in addressing impaired wound healing in diabetic patients.
Liu et al. (Thu,) studied this question.