Platelet-derived respiratory-competent mitochondria transfer to mesenchymal stem cells to promote wound healing via metabolic reprogramming

细胞生物学 间充质干细胞 线粒体 伤口愈合 生物 血管生成 干细胞 免疫学 癌症研究
作者
Enlin Chen,Zhe Chen,Linxi Chen,Xiao Hu
出处
期刊:Platelets [Informa]
卷期号:33 (2): 171-173 被引量:9
标识
DOI:10.1080/09537104.2021.1961717
摘要

Mitochondria regulate intracellular metabolism and are also involved in intercellular transfer in vitro and in vivo, thereby affecting the function of adjacent cells. Mitochondria can also be transferred to various differentiated cells to improve their respiratory function, ATP production, as well as protect damaged cells from apoptosis. Both in vivo and in vitro, mitochondria can be transferred from one cell to another to regulate cellular metabolism under physiological or pathophysiological conditions, referred to as “mitochondrial translocation”. Mitochondrial translocation is associated in various situations such as repairing damaged cells, promoting cancer progression and enhancing chemoresistance. Platelets contain mitochondria that promote energy metabolism and various growth factors, thus playing an important role in pathophysiological processes such as thrombosis, hemostasis, inflammation and wound healing. Current studies suggest that mesenchymal stem cells (MSCs) can communicate with their microenvironment through bidirectional alternation of mitochondria to improve their wound healing capacity. Platelets or platelet-containing preparations such as platelet-rich plasma (PRP) can stimulate the proliferation and pro-angiogenic properties of MSCs under oxidative stress to enhance their survival. Recent studies by Levoux et al. have shown that activated platelet-derived mitochondria have the respiratory capacity to translocate to MSCs and stimulate the pro-angiogenic properties of MSCs through metabolic reprogramming, thereby promoting angiogenesis and wound healing. The mechanism of mitochondrial internalization of cells and energy metabolism is a new example of mitochondrial translocation altering somatic cell behavior and viability. Therefore, we aim to comment the mechanisms of platelet mitochondrial translocation and metabolic reprogramming of MSCs, suggesting that platelets or platelet-containing preparations such as platelet-rich plasma (PRP) may provide a practical guide for tissue injury treatment.
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