Figure 6.

The lncRNA Plscr4 Protected Mitochondrial Function in Response to Hypertrophic Stress

(A) Representative western blot bands of Mitofusin-2 (Mfn2) in the CMs transfected with Plscr4 or the vector control and that were subsequently treated with Ang II (1 μmol/L) for 48 hr (n = 6; *p < 0.05). (B) Representative images of the JC-1 fluorescence. The CMs were transfected with Plscr4 or the vector control and subsequently treated with Ang II (1 μmol/L) for 48 hr, then incubated with JC-1 staining solution. JC-1 exhibited a potential-dependent accumulation in the mitochondria; in healthy cells with a high potential, JC-1 forms complexes emitting a red fluorescence, and in unhealthy cells with a low mitochondrial membrane potential, JC-1 remains in a monomeric form, emitting green fluorescence. The state of the membrane potential was expressed by the ratio of red to green fluorescence (n > 50 cells per experimental group; *p < 0.05). (C) The ROS levels were determined in the CMs that were transfected with Plscr4 or the vector control, subsequently treated with Ang II (1 μmol/L) for 48 hr, and then incubated with the ROS-specific probe DCFH-DA. DCFH-DA could pass through the cell membrane and change into DCFH in the live cells. Intracellular ROS in live cells could interact with DCFH resulting in a fluorometric product DCF, which indicates the amount of ROS present. The cells were imaged with a fluorescence microscope (n > 50 cells per experimental group; *p < 0.05). All of the data are presented as the mean ± SEM.