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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: The diabetic microenvironment causes mitochondrial oxidative stress in glomerular endothelial cells and pathological crosstalk with podocytes

Fig. 3

Diabetic milieu induces increased endonuclease G accumulation in mitochondrial intermembrane space (IMS) and disrupts mitochondrial architecture. a Immunofluorescence detection of endoG-GFP located in the IMS of mGECs cultured in NG, b with CS, c MG132 and with d DS for 48 h. Arrows show endoG clustering. Scale = 20 μm. e Western blot detecting anti-GFP from endoG-GFP whole cell extracts in a-d with β-actin shown as a loading control (n = 3). f Representative transmission electron microscopy images (magnification 7000x, Scale = 1 μm) showing mitochondria (M) in mGEC cultured in NG control shown as elongated mitochondria with dense matrix and densely aligned cristae, N represents nucleus. Below is a higher power images (12,000x, Scale = 0.5 μm), showing clear mitochondrial inner and outer membranes. g Mitochondrial matrix in DS treated mGECs is largely reduced and few cristae remain, outer membrane rupture is seen (open arrow). There are triple and quadruple membrane rings indicative of autophagy and/or mitophagy (*), and a large number of vacuoles were evident (V) and mitochondria with electron dense material (white *). H) DS + mTEMPO treated mGECs show improved mitochondrial architecture with intact outer membrane and inner membrane cristae

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