SASH1, a new potential link between smoking and atherosclerosis

Abstract Objective We have previously reported that SASH1 expression is increased in circulating human monocytes from smokers and was positively correlated with the number of carotid atherosclerotic plaques. The aim of this study was to further validate the link between smoking, SASH1 and atheroscle...

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Bibliographic Details
Published in:Atherosclerosis 2015-10, Vol.242 (2), p.571-579
Main Authors: Weidmann, Henri, Touat-Hamici, Zahia, Durand, Herve, Mueller, Christian, Chardonnet, Solenne, Pionneau, Cedric, Charlotte, Frédéric, Janssen, Klaus-Peter, Verdugo, Ricardo, Cambien, Francois, Blankenberg, Stefan, Tiret, Laurence, Zeller, Tanja, Ninio, Ewa
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Aorta - metabolism
Atherosclerosis
Atherosclerosis - genetics
Atherosclerosis - metabolism
Atherosclerosis - physiopathology
Biochemistry, Molecular Biology
Cardiovascular
CCND1
CCND3
Cell Cycle
Cell Line
Cell Movement
Cell Proliferation
Cyclin D1 - metabolism
Cyclin D3 - metabolism
Cytochrome P-450 CYP1A1 - metabolism
Endothelial Cells - metabolism
Female
Gene Expression Regulation
Gene Silencing
Genomics
Humans
Life Sciences
Male
Middle Aged
Neovascularization, Pathologic
RNA, Small Interfering - metabolism
SASH1
Smoking
Smoking - metabolism
TP53
Transcriptome
Tumor Suppressor Protein p53 - metabolism
Tumor Suppressor Proteins - metabolism
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Summary:Abstract Objective We have previously reported that SASH1 expression is increased in circulating human monocytes from smokers and was positively correlated with the number of carotid atherosclerotic plaques. The aim of this study was to further validate the link between smoking, SASH1 and atherosclerosis within the vascular wall and to assess the impact of SASH1 expression on endothelial cell functions. Method Human carotids with atherosclerotic plaques were obtained from 58 patients (45 of them with known smoking status: smoker, non-smoker, ex-smokers), and were processed for gene expression analyses and immunostaining. To investigate its function, SASH1 was silenced in human aortic endothelial cells (HAECs) using two different siRNA and subcellular localization of SASH1 was determined by immunostaining and subcellular fractionation. Subsequently the transcriptomic analyses and functional experiments (wound healing, WST-1 proliferation or Matrigel assays) were performed to characterize SASH1 function. Results SASH1 was expressed in human vascular cells (HAECs, smooth muscle cells) and in monocytes/macrophages. Its tissue expression was significantly higher in the atherosclerotic carotids of smokers compared to non-smokers (p 
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2015.08.013