ArticleMolecular and cellular biochemistry2012
Heat shock transcription factor 1 inhibits H₂O₂-induced cardiomyocyte death through suppression of high-mobility group box 1.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Enhancing regulatory T-cell function via inhibition of high mobility group box 1 protein signaling in immune thrombocytopenia.Haematologica · 2023Article
- Repair or destruction-an intimate liaison between ubiquitin ligases and molecular chaperones in proteostasis.FEBS letters · 2017Review
- Differential expression of myocardial heat shock proteins in rats acutely exposed to fluoride.Cell stress & chaperones · 2017Article
- Heat shock transcription factor 1 protects against pressure overload-induced cardiac fibrosis via Smad3.Journal of molecular medicine (Berlin, Germany) · 2017Article
- [Effect of heat shock factor 1 on airway hyperresponsiveness and airway inflammation in mice with allergic asthma].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Article
- Doxorubicin attenuates CHIP-guarded HSF1 nuclear translocation and protein stability to trigger IGF-IIR-dependent cardiomyocyte death.Cell death & disease · 2016Article
- Extracellular high-mobility group box 1 mediates pressure overload-induced cardiac hypertrophy and heart failure.Journal of cellular and molecular medicine · 2016Article
- High Mobility Group Box-1: A Missing Link between Diabetes and Its Complications.Mediators of inflammation · 2016Review
- Extracellular heat shock proteins protect U937 cells from H2O2-induced apoptotic cell death.Molecular and cellular biochemistry · 2016Article
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- Innate immunity and cardiomyocytes in ischemic heart disease.Life sciences · 2014Review
- Excessive mechanical stress increases HMGB1 expression in human lung microvascular endothelial cells via STAT3.Microvascular research · 2014Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat shock transcription factor 1 (HSF1), which has been identified as an endogenous cardioprotective factor, possesses considerable anti-inflammatory effects and the ability against oxidative stress. However, the mechanisms have not been fully characterized yet. In this study, we investigated the effects of HSF1-regulated HMGB1 on cardiomyocyte death. Cultured cardiomyocytes were transfected with empty vector or HSF1 plasmid before the exposure to H(2)O(2). Cell death was assessed by cell staining. Additionally, the levels of intracellular and extracellular HMGB1 as well as its subcellular location were detected, and the expression of heat shock proteins (HSP27 and HSP90) in the cardiomyocytes was also determined. Not only did H(2)O(2) significantly increase cell death, but also elevated the levels of intracellular and extracellular HMGB1 and induced its translocation, whereas, as expected, HSF1 overexpression effectively attenuated cell death. Furthermore, HSF1 inhibited the intracellular expression of HMGB1 at early stage of oxidative stress and subsequently, HSF1 did negatively regulate the extracellular levels and the translocation of HMGB1 at late stage. Besides, the expression of HSP27 and HSP90 was significantly increased. These results suggested HSF1-attenuated cardiomyocyte death via reducing intracellular and extracellular levels of HMGB1 as well as preventing its translocation, which was partially associated with HSP27 and HSP90 up-regulated by HSF1 overexpression.
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