Role of heat shock transcription factor 1(HSF1)-upregulated macrophage in ameliorating pressure overload-induced heart failure in mice

Du, Peizhao; Chang, Yaowei; Dai, Fangjie; Wei, Chunyan; Zhang, Qi; Li, Jiming

doi:10.1016/j.gene.2018.04.042

Cited by 9 publications

(6 citation statements)

References 35 publications

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“…Samarasinghe et al ( 26 ) have found that sequestosome 1 (p62/SQSTM1), a protein involved in the delivery of autophagic substrates and nucleation of autophagosomes, is an HSF1-regulated gene. Du et al ( 27 ) found that silencing HSF1 correlated with a reduction in autophagy and thus enhanced cell death. Compared with the wild-type subgroup, the expressions of LC3II/LC3I and Beclin1 were shown to have an obvious increase, and increased autophagosome formation was observed on electron microscopy in the HSF1 transgene (HSF1-TG) subgroup.…”

Section: Discussionmentioning

confidence: 99%

HSF1 Attenuates the Release of Inflammatory Cytokines Induced by Lipopolysaccharide through Transcriptional Regulation of Atg10

Tan

Huang

et al. 2023

Microbiol Spectr

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Section: Discussionmentioning

confidence: 99%

HSF1 Attenuates the Release of Inflammatory Cytokines Induced by Lipopolysaccharide through Transcriptional Regulation of Atg10

Tan

Huang

et al. 2023

Microbiol Spectr

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“…Induction of HSPs in response to chemical and mechanical stress enhances protein folding, inhibits inflammation and apoptosis, and provides cytoskeletal protection (68). While little is known about the role of HSPs in pressure overload-induced heart failure, heat shock factor 1 (HSF-1), the transcription factor that regulates HSPs is induced by TAC in rats and mice, and constitutive activation of HSF-1 ameliorates TAC-induced cardiac hypertrophy, fibrosis and cardiac dysfunction (69)(70)(71).…”

Section: Discussionmentioning

confidence: 99%

Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

Zelko

Dassanayaka

Malovichko

et al. 2021

Preprint

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Benzene is a ubiquitous environmental pollutant abundant in household products, petrochemicals and cigarette smoke. Benzene is a well-known carcinogen in humans and experimental animals; however, little is known about the cardiovascular toxicity of benzene. Recent population-based studies indicate that benzene exposure is associated with an increased risk for heart failure. Nonetheless, it is unclear whether benzene exposure is sufficient to induce and/or exacerbate heart failure. We examined the effects of benzene (50 ppm, 6 h/day, 5 days/week, 6 weeks) or HEPA-filtered air exposure on transverse aortic constriction (TAC)-induced pressure overload in male C57BL/6J mice. Our data show that benzene exposure had no effect on cardiac function in the Sham group; however, it significantly compromised cardiac function as depicted by a significant decrease in fractional shortening and ejection fraction, as compared with TAC/Air-exposed mice. RNA-seq analysis of the cardiac tissue from the TAC/benzene-exposed mice showed a significant increase in several genes associated with adhesion molecules, cell-cell adhesion, inflammation, and stress response. In particular, neutrophils were implicated in our unbiased analyses. Indeed, immunofluorescence studies showed that TAC/benzene exposure promotes infiltration of CD11b+/S100A8+/myeloperoxidase+-positive neutrophils in the hearts by 3-fold. In vitro, the benzene metabolites, hydroquinone and catechol, induced the expression of P-selectin in cardiac microvascular endothelial cells by 5-fold and increased the adhesion of neutrophils to these endothelial cells by 1.5-2.0-fold. Benzene metabolite-induced adhesion of neutrophils to the endothelial cells was attenuated by anti-P-selectin antibody. Together, these data suggest that benzene exacerbates heart failure by promoting endothelial activation and neutrophil recruitment.

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“…Toxicological Sciences ameliorates TAC-induced cardiac hypertrophy, fibrosis and cardiac dysfunction (72)(73)(74).…”

Section: Page 13 Of 26mentioning

confidence: 99%

Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

Zelko

Dassanayaka

Malovichko

et al. 2021

Toxicological Sciences

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Benzene is a ubiquitous environmental pollutant abundant in household products, petrochemicals, and cigarette smoke. Benzene is a well-known carcinogen in humans and experimental animals; however, little is known about the cardiovascular toxicity of benzene. Recent population-based studies indicate that benzene exposure is associated with an increased risk for heart failure. Nonetheless, it is unclear whether benzene exposure is sufficient to induce and/or exacerbate heart failure. We examined the effects of benzene (50 ppm, 6 h/day, 5 days/week, and 6 weeks) or high-efficiency particulate absorbing-filtered air exposure on transverse aortic constriction (TAC)-induced pressure overload in male C57BL/6J mice. Our data show that benzene exposure had no effect on cardiac function in the Sham group; however, it significantly compromised cardiac function as depicted by a significant decrease in fractional shortening and ejection fraction, as compared with TAC/Air-exposed mice. RNA-seq analysis of the cardiac tissue from the TAC/benzene-exposed mice showed a significant increase in several genes associated with adhesion molecules, cell-cell adhesion, inflammation, and stress response. In particular, neutrophils were implicated in our unbiased analyses. Indeed, immunofluorescence studies showed that TAC/benzene exposure promotes infiltration of CD11b+/S100A8+/myeloperoxidase+-positive neutrophils in the hearts by 3-fold. In vitro, the benzene metabolites, hydroquinone, and catechol, induced the expression of P-selectin in cardiac microvascular endothelial cells by 5-fold and increased the adhesion of neutrophils to these endothelial cells by 1.5- to 2.0-fold. Benzene metabolite-induced adhesion of neutrophils to the endothelial cells was attenuated by anti-P-selectin antibody. Together, these data suggest that benzene exacerbates heart failure by promoting endothelial activation and neutrophil recruitment.

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Role of heat shock transcription factor 1(HSF1)-upregulated macrophage in ameliorating pressure overload-induced heart failure in mice

Cited by 9 publications

References 35 publications

HSF1 Attenuates the Release of Inflammatory Cytokines Induced by Lipopolysaccharide through Transcriptional Regulation of Atg10

HSF1 Attenuates the Release of Inflammatory Cytokines Induced by Lipopolysaccharide through Transcriptional Regulation of Atg10

Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

Chronic Benzene Exposure Aggravates Pressure Overload-Induced Cardiac Dysfunction

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