title: HSF1 Relieves Amyloid-β-Induced Cardiomyocytes Apoptosis.
abstract: Accumulation of amyloid-β in organs results in a series of diseases. Heat shock transcription factor 1 (HSF1) is the master regulator of genes encoding molecular chaperones and attenuates apoptosis induced by multiple factors. However, the role of HSF1 on amyloid-β-induced apoptosis is still unknown. The present study was aimed to explore the function of HSF1 in amyloid-β-induced cardiomyocytes apoptosis. TUNEL assay and flow cytometry analysis were used to detect cell apoptosis. Phalloidin staining was used to detect cytoskeleton injury. Changes in expression levels of proteins involved in apoptosis and endoplasmic reticulum stress were measured by Western blot. In our study, amyloid-β was found to promote apoptosis, impair cytoskeleton, and induce endoplasmic reticulum stress in isolated cardiomyocytes. However, these damaging effects of amyloid-β can be relieved by over-expression of HSF1, and the protective role of HSF1 might be associated with the regulation of HSPs expressions. Results of our study suggest that over-expression of HSF1 might become a promising gene therapeutic for the treatment of heart diseases associated with amyloid-β accumulation.
authors: Department of Nephrology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, China. zhangbeiru@hotmail.com.
authors: Beiru
authors: B
authors: Zhang
authors: Department of Nephrology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, China.
authors: Ping
authors: P
authors: He
authors: Department of Neurosurgery, Affiliated Central Hospital of Shenyang Medical College, Shenyang, 110024, Liaoning, China.
authors: Yonghao
authors: Y
authors: Lu
authors: Department of Nephrology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, China.
authors: Xiaohui
authors: X
authors: Bian
authors: Department of Nephrology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, China.
authors: Xu
authors: X
authors: Yang
authors: Department of Pathology, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
authors: Xiaoying
authors: X
authors: Fu
authors: Department of Nephrology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, China.
authors: Yan
authors: Y
authors: Wu
authors: Department of Nephrology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, China.
authors: Detian
authors: D
authors: Li
mesh_terms: D016229:Amyloid beta-Peptides / Q000633:toxicity; D000818:Animals; D017209:Apoptosis; D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress; D000076249:Heat Shock Transcription Factors; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism*; D010446:Peptide Fragments / Q000633:toxicity; D051381:Rats; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D004268:DNA-Binding Proteins; D000076249:Heat Shock Transcription Factors; C000619709:Hsf1 protein, rat; D010446:Peptide Fragments; D014157:Transcription Factors; C074636:amyloid beta-protein (25-35)
keywords: Amyloid-β; Apoptosis; Cardiomyocytes; Heat shock protein; Heat shock transcription factor 1