Exosomes derived from platelet-rich plasma promote diabetic wound healing via the JAK2/STAT3 pathway
Diabetic non-healing wounds are bringing a heavy burden on patients and society. Platelet-rich plasma (PRP) has been widely applied in tissue regenerating for containing various growth factors. Recently, PRP-derived exosomes (PRP-Exos) have been proved to be more effective than PRP in tissue regener...
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Published in | iScience Vol. 26; no. 11; p. 108236 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Inc
17.11.2023
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Diabetic non-healing wounds are bringing a heavy burden on patients and society. Platelet-rich plasma (PRP) has been widely applied in tissue regenerating for containing various growth factors. Recently, PRP-derived exosomes (PRP-Exos) have been proved to be more effective than PRP in tissue regeneration. However, few studies have investigated the therapeutic potential of PRP-Exos in diabetic wound healing to date. Therefore, we extracted and identified exosomes derived from PRP and tested its promoting effect on diabetic wound healing in vivo and in vitro. We found that high glucose (HG) inhibited cell proliferation and migration and induced apoptosis through ROS-dependent activation of the JNK and p38 MAPK signaling pathways. PRP-Exos can stimulate fibroblast functions and accelerate diabetic wound healing. The benefits of PRP-Exos may be attributed to its capability to prevent HG-induced ROS-dependent apoptosis via the PDGF-BB/JAK2/STAT3/Bcl-2 signaling pathway. This illustrates the therapeutic potential of PRP-Exos in diabetic wounds.
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•PRP-Exos could promote fibroblasts proliferation and migration•PRP-Exos alleviate HG-induced apoptosis through JAK2/STAT3/Bcl-2 pathway•PRP-Exos have a protective effect on diabetic wound healing
Cell biology; Cellular physiology; Human metabolism |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally Lead contact |
ISSN: | 2589-0042 2589-0042 |
DOI: | 10.1016/j.isci.2023.108236 |