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. 2024 Oct 26;29:101314. doi: 10.1016/j.mtbio.2024.101314

Fig. 9.

Fig. 9

GPR137 might be a new therapeutic target for random-pattern skin flaps. (A)The expression of GPR137, P-PI3K, PI3K, P-AKT, AKT, P-mTOR, mTOR and LC3B expressions of RPSFs in the Shame, PBS, EXO, FEXOanti-miR−183−5p, FEXO groups. The gels have been run under the same experimental conditions, and cropped blots were used here. (B) Digital image of RPSFs on D7 in Scramble, GPR137, siGPR137, FEXO, FEXOanti-miR−183−5p and FEXOanti-miR−183−5p + GPR137 groups. (C) The percentage of survival area in each group (n = 5). (D) The full field LDBF images of RPSHs in Scramble, GPR137, siGPR137, FEXO, FEXOanti-miR−183−5p and FEXOanti-miR−183−5p + GPR137 groups on D7. (E) The signal intensity of blood flow of flaps was analyzed in each group (n = 5). (F) The immunofluorescence images of CD31/EMCN positive vessels of skin flaps in Scramble, GPR137, siGPR137, FEXO, FEXOanti-miR−183−5p and FEXOanti-miR−183−5p + GPR137 groups. (G) The number of CD31/EMCN positive vessels were analyzed in each group (n = 3). (H–L) The density value of the proteins in OGD endothelial cells in each group (n = 3). (M) The graphical abstract of extracellular vesicles containing miR-183-5p derived from FGF1-pretreated ADSCs protect endothelial cells from oxidative stress, apoptosis and pyroptosis through enhancing autophagy.