Heat‐shock transcription factor 1 is critically involved in the ischaemia‐induced cardiac hypertrophy via JAK2/STAT3 pathway

Figures

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  Figure 1. The phosphorylation of HSF1 was reduced by both MI and hypoxic stimuli. A, Representative Western blots and (B) quantitative results of total and phosphorylation level of HSF1 in the LV border zone of MI 1 wk after LAD ligation. N = 5 per experimental group. MI, myocardial infarction. *P < .05 compared with sham. C, Representative Western blots and (D) quantitative results of total and phosphorylation level of HSF1 in NRCMs stimulated by hypoxia. N = 5 independent experiments. GAPDH was served as internal control. NO, normoxia. HO, hypoxia. All data are expressed as mean ± SEM *P < .05 compared with NO

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  Figure 2. Deficiency of HSF1 deteriorated hypoxia‐induced myocardial hypertrophy in vitro. A,. Representative Western blots of total and phosphorylation level of HSF1 in neonatal cardiomyocytes (NRCMs) after transduced with indicated SiRNA and treated with hypoxia. N = 5 independent experiments. B,. Quantitative results of total and phosphorylation level of HSF1in NRCMs. C and D,. The representative images and quantification data of cardiomyocyte surface area (CSA) of NRCMs stained by α‐myosin heavy chain (α‐MHC). Scale bar: 20 μm. E, mRNA levels of hypertrophic markers, atrial natriuretic peptide (ANP), B‐type natriuretic peptide (BNP) in NRCMs measured by real‐time PCR. GAPDH was served as internal control. F and G,. The TUNEL staining and quantified data of NRCMs. Scale bar: 20 μm. N = 5 independent experiments. NO, normoxia. HO, hypoxia. All data are expressed as mean ± SEM *P < .05 compared with NO + AdshSiRNA, # P < .05 compared with HO + AdshSiRNA

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  Figure 3. Deficiency of HSF1 aggravated cardiac hypertrophy induced by MI in mice. A, Heart weight/body weight ratio (HW/BW) (B) left ventricular weight/tibia length ratio (LVW/TL) and (C) lung weight/tibia length ratio (LW/TL) of mice. D, Representative images of histological sections of the mouse LVs were stained with haematoxylin‐eosin (H&E) 1 wk after MI or sham surgery. Scale bar: 50 μm. E, Quantitative results of the cross‐sectional area (CSA) of mouse cardiomyocytes quantified using an image analysis system. F,. Real‐time PCR analysis of ANP and BNP in mouse border zone area of LVs 1 wk after MI. G, the infarction size of the mouse hearts. H and I, The TUNEL staining and quantified data of mouse hearts. Scale bar: 20 μm. GAPDH was served as internal control. N = 7‐8 per experimental group. All data are expressed as mean ± SEM *P < .05, **P < .01 compared with WT sham, # P < .05, ## P < .01 compared with WT MI

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  Figure 4. HSF1 regulated the JAK2/STAT3 signalling pathway. A, Representative Western blots and (B) and (C) the quantitative results of total and phosphorylation level of JAK2 and STAT3 in the border zone area of mouse left ventricles (LVs) 1 wk after MI or sham surgery. N = 5 independent experiments in all groups. *P < .05, **P < .01 vs WT sham, # P < .05 vs WT MI. D, Representative Western blots and (E) and (F) the quantitative result of total and phosphorylation level of JAK2 and STAT3 in NRCMs treated by hypoxia and indicated SiRNA. N = 5 per experimental group. All data are expressed as mean ± SEM **P < .01 compared with NO + AdshRNA, # P < .05, ## P < .01 compared with HO + AdshRNA

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  Figure 5. Enhance of HSF1 attenuated cardiac hypertrophy induced by MI in mice. A, Heart weight/body weight ratio (HW/BW), (B) left ventricular weight/tibia length ratio (LVW/TL) and (C) lung weight/tibia length ratio (LW/TL) of mice. D, Representative images of histological sections of the mouse LVs were stained with haematoxylin‐eosin (H&E) 1 wk after MI or sham surgery. Scale bar: 50 μm. E, Quantitative results of the cross‐sectional area (CSA) of mouse cardiomyocytes quantified using an image analysis system. F, Real‐time PCR analysis of ANP and BNP in mouse border zone area of LVs 1 wk after MI. (G) The infarction size of the mouse hearts. H and I, The TUNEL staining and quantified data of mouse hearts. Scale bar: 50μm. GAPDH was served as internal control. N = 7 per experimental group. All data are expressed as mean ± SEM *P < .05, **P < .01 compared with WT sham, # P < .05, ## P < .01 compared with WT MI