Figure 4.

Overexpression of Plscr4 Mitigates Pressure Overload-Induced Cardiac Hypertrophy

(A) The specific overexpression of lncRNA-plscr4 in the mouse heart was verified. The mice were injected through the tail vein with AAV9 viral particles carrying Plscr4 or a vector for 3 weeks, and then they were subjected to TAC or sham operation for 4 weeks (n = 6; *p < 0.05 versus sham). (B) The statistical results for the HW/BW, lung weight (LW)/HW, and HW/tibia length (TL) ratios in the sham or TAC mice infected with the AAV9-Vector or AAV9-Plscr4 (n = 6; *p < 0.05). (C) Representative histological results of the H&E staining, Masson staining to assess fibrosis, and wheat germ agglutinin (WGA) staining of the mouse heart tissues. The AAV9-Vector- and AAV9-Plscr4-overexpressing mice underwent 4 weeks of the TAC or sham operation. Then the mice hearts were collected and fixed in 4% paraformaldehyde for 24 hr followed by embedding in paraffin, and they were cut into 5-μm-thick cross-sectional slices. The slices were stained by H&E, Masson trichrome, and WGA. (D) The relative mRNA levels of the hypertrophic markers ANP, BNP, and β-MHC in the AAV9-Vector- and AAV9-Plscr4-overexpressing mice after 4 weeks of the TAC or sham operation (n = 6; *p < 0.05 versus sham + AAV9-Vector, ^#p < 0.05 versus TAC + AAV9-Vector). (E) Representative western blot bands of β-MHC in the AAV9-Vector- and AAV9-Plscr4-overexpressing mice after 4 weeks of the TAC or sham operation (n = 6; *p < 0.05).