Heat shock transcription factor 1 protects heart after pressure overload through promoting myocardial angiogenesis in male mice

Zou, Yunzeng; Li, Jiming; Ma, Hong; Jiang, Hong; Yuan, Jie; Gong, Hui; Liang, Yanyan; Guan, Aili; Wu, Jian; Li, Lei; Zhou, Ning; Niu, Yuhong; Sun, Aijun; Nakai, Asami; Wang, Ping; Takano, Hiroyuki; Komuro, Issei; Ge, Junbo

doi:10.1016/j.yjmcc.2011.07.030

Cited by 42 publications

(49 citation statements)

References 30 publications

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“…[35][36][37] In unstressed cells, HSF1 is present in both the cytoplasm and the nucleus. In response to stress stimuli, HSF1 accumulates within the The activation of SIRT1 maintained HSF1 in the deacetylated active state and prolonged its binding to HSEs.…”

Section: Discussionmentioning

confidence: 99%

ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

Huang

et al. 2014

Cell Death Differ

115

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Hypertension-induced cardiac hypertrophy and apoptosis are major characteristics of early-stage heart failure. Our previous studies found that the activation of insulin-like growth factor receptor II (IGF-IIR) signaling was critical for hypertensive angiotensin II (ANG II)-induced cardiomyocyte apoptosis. However, the detailed mechanism by which ANG II regulates IGF-IIR in heart cells remains elusive. In this study, we found that ANG II activated its downstream kinase JNK to increase IGF-IIR expression through the ANG II receptor angiotensin type 1 receptor. JNK activation subsequently led to sirtuin 1 (SIRT1) degradation via the proteasome, thus preventing SIRT1 from deacetylating heat-shock transcription factor 1 (HSF1). The resulting increase in the acetylation of HSF1 impaired its ability to bind to the IGF-IIR promoter region (nt À 748 to À 585). HSF1 protected cardiomyocytes by acting as a repressor of IGF-IIR gene expression, and ANG II diminished this HSF1-mediated repression through enhanced acetylation, thus activating the IGF-IIR apoptosis pathway. Taken together, these results suggest that HSF1 represses IGF-IIR gene expression to protect cardiomyocytes. ANG II activates JNK to degrade SIRT1, resulting in HSF1 acetylation, which induces IGF-IIR expression and eventually results in cardiac hypertrophy and apoptosis. HSF1 could be a valuable target for developing treatments for cardiac diseases in hypertensive patients. Apoptosis has been implicated in a wide variety of cardiovascular disorders, including myocardial infarction and heart failure, suggesting that activation of apoptotic pathways contributes to cardiomyocyte loss and subsequently cardiac dysfunction. Previous studies reported that several extracellular molecules, such as insulin-like growth factors (IGFs) and angiotensin II (ANG II), are involved in the development of cardiac hypertrophy and apoptosis.

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Section: Discussionmentioning

confidence: 99%

ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

Huang

et al. 2014

Cell Death Differ

115

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“…Pressure overload was imposed on the heart of mice by transverse aortic constriction (TAC), as we described previously 14, 15. Recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) (Hmgbiotech, Milano, Italy) or PBS was injected into the LV wall, as described previously 9, 16.…”

Section: Methodsmentioning

confidence: 99%

“…Echocardiographic analyses were performed before (baseline) and at 2 and 4 weeks post TAC in mice, as we described previously 14, 19. Briefly, Transthoracic echocardiography was performed with an animal specific instrument (Vevo770; VisualSonics, Toronto, ON, Canada).…”

Section: Methodsmentioning

confidence: 99%

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Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure

Zhang

Liu

Jiang

et al. 2015

J Cellular Molecular Medi

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Inflammation plays a key role in pressure overload‐induced cardiac hypertrophy and heart failure, but the mechanisms have not been fully elucidated. High‐mobility group box 1 (HMGB1), which is increased in myocardium under pressure overload, may be involved in pressure overload‐induced cardiac injury. The objectives of this study are to determine the role of HMGB1 in cardiac hypertrophy and cardiac dysfunction under pressure overload. Pressure overload was imposed on the heart of male wild‐type mice by transverse aortic constriction (TAC), while recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the LV wall. Moreover, cardiac myocytes were cultured and given sustained mechanical stress. Transthoracic echocardiography was performed after the operation and sections for histological analyses were generated from paraffin‐embedded hearts. Relevant proteins and genes were detected. Cardiac HMGB1 expression was increased after TAC, which was accompanied by its translocation from nucleus to both cytoplasm and intercellular space. Exogenous HMGB1 aggravated TAC‐induced cardiac hypertrophy and cardiac dysfunction, as demonstrated by echocardiographic analyses, histological analyses and foetal cardiac genes detection. Nevertheless, the aforementioned pathological change induced by TAC could partially be reversed by HMGB1 inhibition. Consistent with the in vivo observations, mechanical stress evoked the release and synthesis of HMGB1 in cultured cardiac myocytes. This study indicates that the activated and up‐regulated HMGB1 in myocardium, which might partially be derived from cardiac myocytes under pressure overload, may be of crucial importance in pressure overload‐induced cardiac hypertrophy and cardiac dysfunction.

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“…The therapeutic potential of targeting tumor endothelium and vascular supply is now widely recognized; solid tumors cannot grow beyond the size of a few millimeters without inducing the proliferation of endothelium and formation of new blood vessels [19]. HSF1 promotes cardiac angiogenesis through suppressing p53 and downstream upregulation of hypoxia-inducible factor-1a to maintain cardiac adaptation [20]. In another pathway, HSF1 contributed to ischemia-induced angiogenesis by regulating the mobilization of bone marrow stem/progenitor cells in cardiovascular disease [21].…”

mentioning

confidence: 99%

Upregulation of Nuclear Heat Shock Factor 1 Contributes to Tumor Angiogenesis and Poor Survival in Patients With Non–Small Cell Lung Cancer

Cui

Tian

Chen

2015

The Annals of Thoracic Surgery

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Heat shock transcription factor 1 protects heart after pressure overload through promoting myocardial angiogenesis in male mice

Cited by 42 publications

References 30 publications

ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

ANG II promotes IGF-IIR expression and cardiomyocyte apoptosis by inhibiting HSF1 via JNK activation and SIRT1 degradation

Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure

Upregulation of Nuclear Heat Shock Factor 1 Contributes to Tumor Angiogenesis and Poor Survival in Patients With Non–Small Cell Lung Cancer

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