title: Mechanical stretch changes coronary artery fibroblasts function by upregulating HSF1 protein expression.
abstract: The study is designed to investigate effect of mechanical stretch on the function of fibroblast cells. Human coronary artery fibroblasts were cultured. They were divided into two groups: stretch group (stretch for 24h) and no-stretch group (did not stretch). ELISA analysis was used for detection of collagen secretion. CCK-8 method was used for detection of cells proliferation. RT-PCR method was used for detection of MMP, TIMP, IL-6, alpha-SMA, HSF1 and HSP70 mRNA expression. Western-blotting method was used for detection of HSF1 protein expression. Results showed that cells proliferation in stretch group was stronger than that in no-stretch group. Hydroxyproline secretion in stretch group was more than that in no-stretch group. MMP-9/TIMP, alpha-SMA, IL-6, HSF1 and HSP70 in stretch group was higher than those in no-stretch group. Western-blotting analysis showed that HSF1 protein expression was upregulated in stretch group. It can be concluded that mechanical stretch changed human coronary artery fibroblasts cells proliferation, collagen formation, the secretion of inflammatory factor possibly by upregulating HSF1 protein expression.
authors.affiliation: Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China. lxb70@hotmail.com
authors.forename: Jiming
authors.initials: J
authors.lastname: Li
authors.forename: Yibo
authors.initials: Y
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Cui
authors.forename: Jie
authors.initials: J
authors.lastname: Wang
authors.forename: Xiufeng
authors.initials: X
authors.lastname: Pang
authors.forename: Yan
authors.initials: Y
authors.lastname: Lai
authors.forename: Yian
authors.initials: Y
authors.lastname: Yao
authors.forename: Xuebo
authors.initials: X
authors.lastname: Liu
authors.forename: Ying
authors.initials: Y
authors.lastname: Li
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D049109:Cell Proliferation; D002478:Cells, Cultured; D003094:Collagen / Q000235:genetics / Q000378:metabolism; D003331:Coronary Vessels / Q000166:cytology / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D005347:Fibroblasts / Q000166:cytology / Q000502:physiology*; D005786:Gene Expression Regulation; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D000076249:Heat Shock Transcription Factors; D006801:Humans; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D040542:Mechanotransduction, Cellular / Q000502:physiology*; D013314:Stress, Mechanical; D019714:Tissue Inhibitor of Metalloproteinases / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D004268:DNA-Binding Proteins; C000619706:HSF1 protein, human; D018840:HSP70 Heat-Shock Proteins; D000076249:Heat Shock Transcription Factors; C508600:IL6 protein, human; D015850:Interleukin-6; D019714:Tissue Inhibitor of Metalloproteinases; D014157:Transcription Factors; D003094:Collagen; D020780:Matrix Metalloproteinase 9