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Computational modelling suggests good, bad and ugly roles of glycosaminoglycans in arterial wall mechanics and mechanobiology.
MedLine Citation:
PMID:  24920112     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
The medial layer of large arteries contains aggregates of the glycosaminoglycan hyaluronan and the proteoglycan versican. It is increasingly thought that these aggregates play important mechanical and mechanobiological roles despite constituting only a small fraction of the normal arterial wall. In this paper, we offer a new hypothesis that normal aggregates of hyaluronan and versican pressurize the intralamellar spaces, and thereby put into tension the radial elastic fibres that connect the smooth muscle cells to the elastic laminae, which would facilitate mechanosensing. This hypothesis is supported by novel computational simulations using two complementary models, a mechanistically based finite-element mixture model and a phenomenologically motivated continuum hyperelastic model. That is, the simulations suggest that normal aggregates of glycosaminoglycans/proteoglycans within the arterial media may play equally important roles in supporting (i.e. a structural role) and sensing (i.e. an instructional role) mechanical loads. Additional simulations suggest further, however, that abnormal increases in these aggregates, either distributed or localized, may over-pressurize the intralamellar units. We submit that these situations could lead to compromised mechanosensing, anoikis and/or reduced structural integrity, each of which represent fundamental aspects of arterial pathologies seen, for example, in hypertension, ageing and thoracic aortic aneurysms and dissections.
Authors:
S Roccabianca; C Bellini; J D Humphrey
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of the Royal Society, Interface / the Royal Society     Volume:  11     ISSN:  1742-5662     ISO Abbreviation:  J R Soc Interface     Publication Date:  2014 Aug 
Date Detail:
Created Date:  2014-06-12     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101217269     Medline TA:  J R Soc Interface     Country:  England    
Other Details:
Languages:  eng     Pagination:  -     Citation Subset:  IM    
Copyright Information:
© 2014 The Author(s) Published by the Royal Society. All rights reserved.
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