Peroxiredoxin‐5 Knockdown Accelerates Pressure Overload‐Induced Cardiac Hypertrophy in Mice

Figures

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  Figure 1. Prx5 expression is increased in hypertrophic hearts and isolated NRCMs. (a) The expression of Prx5 in heart tissues was measured by Western blotting and RT-PCR (n = 4, ∗P < 0.05 vs. the sham group). (c) The expression of Prx5 in heart tissues was measured by Western blotting and RT-PCR (n = 4, ∗P < 0.05 vs. the PBS group).

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  Figure 2. Prx5 knockdown accelerates pressure overload-induced cardiac hypertrophy. (a) The levels of Prx5 after injection with AAV9-shPrx5 (n = 4). (b) Results for the HW/BW ratio, HW/TL ratio, LW/BW ratio, LW/TL ratio, and CSA of each group (n = 6). (c) HE and WGA staining were performed in each group (n = 6; scale bar, 50 μm). (d) The expression of ANP, BNP, β-MHC, and Myh7 was measured by RT-PCR in each group (n = 5). ∗P < 0.05 vs. the sham group; #P < 0.05 vs. the TAC group.

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  Figure 3. Prx5 knockdown accelerates pressure overload-induced cardiac fibrosis. (a) PSR staining was performed in each group (n = 6; scale bar, 50 μm). (b) The expression of collagen I, collagen III, TGF-β, and CTGF was measured by RT-PCR in each group (n = 6). ∗P < 0.05 vs. the sham group; #P < 0.05 vs. the TAC group.

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  Figure 4. Prx5 knockdown accelerates pressure overload-induced oxidative stress and apoptosis. (a) DHE staining was performed in each group (n = 5; scale bar, 100 μm). (b) Quantitative results of SOD activity and GSH, MDA, and H2O2 levels in the hearts of each group (n = 6). ∗P < 0.05 vs. the sham group; #P < 0.05 vs. the TAC group.

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  Figure 5. Prx5 knockdown accelerates pressure overload-induced apoptosis in mice. (a) TUNEL staining was performed in each group (n = 4; scale bar, 50 μm). (b) The expression of Bax and Bcl-2 was measured by Western blot in each group (n = 4). ∗P < 0.05 vs. the sham group; #P < 0.05 vs. the TAC group.

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  Figure 6. Prx5 knockdown accelerates AngII-induced cardiomyocyte hypertrophy in vitro. (a) The levels of Prx5 were measured by Western blot (n = 4). (b) Immunofluorescence staining for α-actinin was performed in each group (n = 4; scale bar, 25 μm). (c) The expression of ANP, BNP, β-MHC, and Myh7 was measured by RT-PCR in each group (n = 6). ∗P < 0.05 vs. the PBS group; #P < 0.05 vs. the AngII group.

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  Figure 7. Prx5 knockdown accelerates AngII-induced oxidative stress and apoptosis in vitro. (a) Quantitative results of SOD activity and GSH, MDA, and H2O2 levels in the hearts of each group (n = 6). (c) TUNEL staining was performed in each group (n = 4; scale bar, 50 μm). ∗P < 0.05 vs. the PBS group; #P < 0.05 vs. the AngII group.

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  Figure 8. Effect of Prx5 on the MAPK signaling pathway. (a) The expression of p-ERK, t-ERK, p-JNK, t-JNK, p-p38, and p38 in the heart was measured by Western blotting (n = 4). (b) The expression of p-ERK, ERK, p-JNK, JNK, p-p38, and p38 in NVCMs was measured by Western blotting (n = 4). ∗P < 0.05 vs. the sham or PBS group; #P < 0.05 vs. the TAC or AngII group.