Skip to main content
. 2020 Jan 31;318(4):F878–F887. doi: 10.1152/ajprenal.00567.2019

Fig. 4.

Fig. 4.

Mitofusin-2 (Mfn2) is downregulated in mouse ischemic acute kidney injury and in ATP-depleted rat kidney proximal tubular cells (RPTCs). A: human embryonic kidney (HEK)-293 cells were transfected with empty vector or microRNA-214 (miR-214) plasmids. Representative immunoblots and densitometry analysis of Mfn2 demonstrated that miR-214 suppressed Mfn2 expression in HEK-293 cells compared with empty vector (n = 3). B: male C57BL/6J mice were subjected to 25 min of bilateral renal ischemia followed by 48 h of reperfusion (I25/48h) or were subjected to sham operation. Representative immunoblots and densitometry analysis demonstrated the decrease of Mfn2 expression after ischemia-reperfusion (n = 5). β-Actin was used as a loading control. C: RPTCs were treated with 10 mM azide for 3 h to induce ATP depletion and then recovered for 2 h in full culture medium. Representative immunoblots and densitometry analysis of Mfn2 demonstrated Mfn2 downregulation in ATP-depleted RPTCs (n = 3). β-Actin was used as a loading control. Con, control; I/R, ischemia-reperfusion. *P < 0.05; **P < 0.01.