What is it about?
Heat Shock Protein 27 (HSP27) is an endogenous protein that functions in the extracellular space to reduce the formation of hardening of the arteries ("atherosclerosis"). In this paper we show how HSP27 works. First, it activates NF-kB signaling via the TLR4 receptor. Second, this activation results in a marked increase in GM-CSF expression & secretion. Third, GM-CSF augments reverse cholesterol transport, by increasing ABC transporter expression.
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Why is it important?
- This paper shows one means by which HSP27 reduces the build up of cholesterol in atherosclerotic (arterial) plaques. - This paper dissects the role of HSP-27 signaling in macrophages followed the impact of GM-CSF release augmenting reverse cholesterol transport.
Perspectives
Latest publication from O'Brien lab on HSP27 atheroprotection via augmentation of reverse cholesterol transport
Dr Ed O'Brien
University of Calgary Cumming School of Medicine
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Heat shock protein 27–derived atheroprotection involves reverse cholesterol transport that is dependent on GM-CSF to maintain ABCA1 and ABCG1 expression in ApoE
−/−
mice
, The FASEB Journal, February 2017, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201601188r.
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