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Functional screening of mammalian mechanosensitive genes using Drosophila RNAi library- Smarcd3/Bap60 is a mechanosensitive pro-inflammatory gene.

Sci Rep. 2016 Nov 07;6:36461
Sandeep Kumar 1 , In-Hwan Jang 1 , Chan Woo Kim 1 , Dong-Won Kang 1 , Won Jae Lee 2 , Hanjoong Jo 3
Sandeep Kumar 1 , In-Hwan Jang 1 , Chan Woo Kim 1 , Dong-Won Kang 1 , Won Jae Lee 2 , Hanjoong Jo 3
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Author information
  • 1 Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
  • 2 National Creative Research Initiative Center for Hologenomics, and School of Biological Sciences, Seoul National University, Seoul 151-742, South Korea.
  • 3 Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA, USA.
全文

摘要


Disturbed blood flow (d-flow) induces atherosclerosis by altering the expression of mechanosensitive genes in the arterial endothelium. Previously, we identified >580 mechanosensitive genes in the mouse arterial endothelium, but their role in endothelial inflammation is incompletely understood. From this set, we obtained 84 Drosophila lines that silences the target gene under the control of upstream activation sequence (UAS) promoter. These lines were crossed with C564-GAL4 flies expressing GFP under the control of drosomycin promoter, an NF-κB target gene and a marker of pathogen-induced inflammation. Silencing of psmd12 or ERN1 decreased infection-induced drosomycin expression, while Bap60 silencing significantly increased the drosomycin expression. Interestingly, knockdown of Bap60 in adult flies using temperature-inducible Bap60 duanyu1615 enhanced drosomycin expression upon Gram-positive bacterial challenge but the basal drosomycin expression remained unchanged compared to the control. In the mammalian system, smarcd3 (mammalian ortholog of Bap60) expression was reduced in the human- and mouse aortic endothelial cells exposed to oscillatory shear in vitro as well as in the d-flow regions of mouse arterial endothelium in vivo. Moreover, siRNA-mediated knockdown of smarcd3 induced endothelial inflammation. In summary, we developed an in vivo Drosophila duanyu1615 screening method to identify flow-sensitive genes that regulate endothelial inflammation.