HSF1 deficiency accelerates the transition from pressure overload-induced cardiac hypertrophy to heart failure through endothelial miR-195a-3p-mediated impairment of cardiac angiogenesis

Wang, Shijun; Wu, Jian; You, J. Q.; Shi, Hongyu; Xue, Xiaoyu; Huang, Jiayuan; Xu, Lei; Jia, Guanghong; Yuan, Lingyan; Gong, Xue; Luo, Haiyan; Ge, Junbo; Cui, Zhaoqiang; Zou, Yunzeng

doi:10.1016/j.yjmcc.2018.03.017

Cited by 26 publications

(26 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Reduced expression of miR-126 in endothelial progenitor cells independently predicted the outcome of patients with chronic heart failure (92, 93). A role for miRNA based gene regulation in the negative control of cardiac angiogenesis during hypertrophy was also demonstrated for miR-124 (main target: the tetraspanin CD151) (94), miR-195a-3p (main targets: CD31, eNOS, VEGF) (95), miR-320 (main targets: IGF-1, Hsp20 and ETS2) (96) and miR-665 (main target: CD34 expressed on hematopoietic and endothelial cells) (97). Importantly, silencing of miR-652 (targeting the Notch1 ligand Jagged1) was found to stabilize cardiac angiogenesis and prevent heart failure in mice with established hypertrophy following aortic banding (98).…”

Section: Growth Factor Signaling Involved In the Regulation Cardiac Amentioning

confidence: 91%

Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure

Gogiraju

Bochenek

Schäfer

2019

Front. Cardiovasc. Med.

108

View full text Add to dashboard Cite

Endothelial cells are, by number, one of the most abundant cell types in the heart and active players in cardiac physiology and pathology. Coronary angiogenesis plays a vital role in maintaining cardiac vascularization and perfusion during physiological and pathological hypertrophy. On the other hand, a reduction in cardiac capillary density with subsequent tissue hypoxia, cell death and interstitial fibrosis contributes to the development of contractile dysfunction and heart failure, as suggested by clinical as well as experimental evidence. Although the molecular causes underlying the inadequate (with respect to the increased oxygen and energy demands of the hypertrophied cardiomyocyte) cardiac vascularization developing during pathological hypertrophy are incompletely understood. Research efforts over the past years have discovered interesting mediators and potential candidates involved in this process. In this review article, we will focus on the vascular changes occurring during cardiac hypertrophy and the transition toward heart failure both in human disease and preclinical models. We will summarize recent findings in transgenic mice and experimental models of cardiac hypertrophy on factors expressed and released from cardiomyocytes, pericytes and inflammatory cells involved in the paracrine (dys)regulation of cardiac angiogenesis. Moreover, we will discuss major signaling events of critical angiogenic ligands in endothelial cells and their possible disturbance by hypoxia or oxidative stress. In this regard, we will particularly highlight findings on negative regulators of angiogenesis, including protein tyrosine phosphatase-1B and tumor suppressor p53, and how they link signaling involved in cell growth and metabolic control to cardiac angiogenesis. Besides endothelial cell death, phenotypic conversion and acquisition of myofibroblast-like characteristics may also contribute to the development of cardiac fibrosis, the structural correlate of cardiac dysfunction. Factors secreted by (dysfunctional) endothelial cells and their effects on cardiomyocytes including hypertrophy, contractility and fibrosis, close the vicious circle of reciprocal cell-cell interactions within the heart during pathological hypertrophy remodeling.

show abstract

Section: Growth Factor Signaling Involved In the Regulation Cardiac Amentioning

confidence: 91%

Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure

Gogiraju

Bochenek

Schäfer

2019

Front. Cardiovasc. Med.

108

View full text Add to dashboard Cite

show abstract

“…10,11 Prior studies showed that HSF1 has a cardiac protective role as it prevents myocardial fibrosis and pathological cardiac hypertrophy during ischaemia injury and pressure overload. 15,16 In the xenograft model, down-regulation of nuclear HSF1 inhibits the expression of HIF-1α, thereby inhibiting tumour angiogenesis and delaying the development of cancer in patients with lung cancer. For instance, in the chronic pressure-overload mouse model, HSF1 deficiency inhibits angiogenesis and promotes the transition from pressure overload-induced cardiac hypertrophy to heart failure, which is ascribed to the inhibition of the HIF-1α pathway.…”

Section: H Y P E R T E N S I O N C O N T R I B U T E S T O T H E M O mentioning

confidence: 99%

“…16,18 Each measurement was presented as an average of five consecutive cardiac cycles, which were recorded by 3 experienced technicians who were blinded to the mice group allocation. 16,18 Each measurement was presented as an average of five consecutive cardiac cycles, which were recorded by 3 experienced technicians who were blinded to the mice group allocation.…”

Section: Haemodynamic Measurements and Echocardiographymentioning

confidence: 99%

“…were recorded as reported in a previous study. 16,18 Each measurement was presented as an average of five consecutive cardiac cycles, which were recorded by 3 experienced technicians who were blinded to the mice group allocation. The haemodynamic examination was carried out using a 1.4-F pressure catheter (SPR 671, Millar Instruments) advanced into the aorta to reach the LV via the right common carotid artery.…”

Section: Pressure-overload Model and Experimental Protocolmentioning

confidence: 99%

“…For instance, in the chronic pressure-overload mouse model, HSF1 deficiency inhibits angiogenesis and promotes the transition from pressure overload-induced cardiac hypertrophy to heart failure, which is ascribed to the inhibition of the HIF-1α pathway. 15,16 In the xenograft model, down-regulation of nuclear HSF1 inhibits the expression of HIF-1α, thereby inhibiting tumour angiogenesis and delaying the development of cancer in patients with lung cancer. 17 We previously found that HSF1 has a pivotal function in the adaptive mechanism of exercise-induced physiological cardiac hypertrophy and pressure overload-induced pathological cardiac hypertrophy.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Heat shock transcription factor 1 regulates exercise‐induced myocardial angiogenesis after pressure overload via HIF‐1α/VEGF pathway

Tian

Zhou

Yuan

et al. 2020

J Cellular Molecular Medi

Self Cite

View full text Add to dashboard Cite

Exercise training is believed to have a positive effect on cardiac hypertrophy after hypertension. However, its mechanism is still not fully understood. Herein, our findings suggest that heat shock transcription factor 1 (HSF1) improves exercise-initiated myocardial angiogenesis after pressure overload. A sustained narrowing of the diagonal aorta (TAC) and moderately-intense exercise training protocol were imposed on HSF1 heterozygote (KO) and their littermate wild-type (WT) male mice. After two months, the cardiac function was assessed using the adaptive responses to exercise training, or TAC, or both of them such as catheterization and echocardiography. The HE stains assessed the area of myocyte cross-sectional. The Western blot and realtime PCR measured the levels of expression for heat shock factor 1 (HSF1), vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1 alpha (HIF-1α) in cardiac tissues. The anti-CD31 antibody immunohistochemical staining was done to examine how exercise training influenced cardiac ontogeny. The outcome illustrated that exercise training significantly improved the cardiac ontogeny in TAC mice, which was convoyed by elevated levels of expression for VEGF and HIF-1α and preserved the heart microvascular density. More importantly, HSF1 deficiency impaired these effects induced by exercise training in TAC mice. In conclusion, exercise training encourages cardiac ontogeny by means of HSF1 activation and successive HIF-1α/ VEGF up-regulation in endothelial cells during continued pressure overload. K E Y W O R D Scardiac angiogenesis, exercise training, HSF1, pressure overload | 2179 TIAN eT Al.

show abstract

Protective role of heat shock transcription factor 1 in heart failure: A diagnostic approach

Haybar

Shahrabi

Rezaeeyan

et al. 2018

Journal Cellular Physiology

View full text Add to dashboard Cite

Objective Nonexpression or expression inhibition of protective factors has been determined in the occurrence of heart failure (HF). Heat shock transcription factor 1 (HSF1) is among such factors, which reduces the incidence of HF by controlling cardiac hypertrophy and fibrosis. In this study, molecular mechanisms for nonexpression of HSF1 in HF patients have been investigated. Materials and methods This review paper is based on the material obtained via PubMed search of 1996–2018. The key search terms were "heart failure," "heat shock transcription factor 1," "hypertrophy", "fibrosis," and "apoptosis." Results Although factors such as janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and heat shock proteins (HSPs) may respectively increase and decrease susceptibility to HF, in some circumstances, these factors may unexpectedly prevent HF progression. Conclusion Finally, identification of molecular pathways expressed by various factors could be used to design appropriate treatments or to employ strategies inducing the expression of HSF1 to prevent HF.

show abstract

HSF1 deficiency accelerates the transition from pressure overload-induced cardiac hypertrophy to heart failure through endothelial miR-195a-3p-mediated impairment of cardiac angiogenesis

Cited by 26 publications

References 58 publications

Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure

Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure

Heat shock transcription factor 1 regulates exercise‐induced myocardial angiogenesis after pressure overload via HIF‐1α/VEGF pathway

Protective role of heat shock transcription factor 1 in heart failure: A diagnostic approach

Contact Info

Product

Resources

About