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Fig. 2 | BMC Nephrology

Fig. 2

From: Anti-fibrotic potential of erythropoietin signaling on bone marrow derived fibrotic cell

Fig. 2

EPO reduced mitochondrial ROS production and attenuated mitochondrial membrane depolarization in TGF-β stimulated fibrocyte. Recent studies revealed the pathogenesis of mitochondria in organ fibrosis. We analyzed mitochondrial ROS production by mito-SOX reagent in bone marrow derived fibrotic cells. TGF-β stimulation increased mitochondrial ROS production as compared to no stimulated cells. The mitochondrial production of ROS was reduced by EPO signaling (a). Flow cytometry analysis also showed higher frequency of mito-SOX positive cells in TGF-β stimulated group. EPO treatment decreased the frequency of those cells (b). Mmembrane potential (MMP) were measured with JC-1 reagent. JC-1 red indicated mitochondria with high membrane potential, whereas JC-1 green indicated those with low membrane potential. TGF-β stimulation lowered MMP, that was attenuated by EPO signaling (c)

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