Fig. 6.

The mitochondrial redox regulator Mpv17-like and the metalloproteinase inhibitor Reck are miR-21 targets in kidney injury and are important endogenous inhibitors of injury and fibrosis. (A) Photomicrographs showing expression of Mpv17-like. (B) Q-PCR for Mpv17l transcripts normalized to Gapdh in miR-21^-/- or miR-21^+/+ matched mice. (C) Western blot Mpv17l in UUO kidneys from miR-21^-/- or miR-21^+/+ matched mice. (D-E) Images (D) and quantification (E) of ROS production as detected by the oxidized derivative of deoxyguanosine in nuclei of kidney cells in miR-21^-/- or miR-21^+/+matched mice. (F) Photomicrographs showing expression of Reck. (G-H) Q-PCR for Reck transcripts normalized to Gapdh (G) Western blot for Reck (H) in normal or UUO kidneys from miR-21^-/- or miR-21^+/+ matched mice. (J-K) Gelatin zymography (J) and band density quantification (K) of whole cell lysates from UUO kidneys from miR-21^-/- or miR-21^+/+ matched mice. (L-N) Hypoxia studies on primary kidney epithelial cells cultures showing Q-PCR (L-M) and Western blots (N) for Mpv17l and Reck. (n= 3-7/group. * P<0.05, **P<0.01. Bar = 100μm).