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Journal of the American Heart Association

Clinical Articles, News & Views

Heterogenic endothelial responses to inflammation

There is a critical role for the vascular bed of origin in controlling endothelial responses and function to inflammatory stimuli, and bed‐specific expression of N‐linked sugars may provide a signature for select leukocyte recruitment, according to a study1 published recently in the Journal of the American Heart Association.

Authors exposed human endothelial cells isolated from five systemic arterial beds from one donor (to overcome donor‐to‐donor genetic/epigenetic differences), the umbilical vein, and pulmonary microvasculature to TNF‐α, LPS, and IL‐1β and assessed acute (ERK1/2 and p65) and chronic (ICAM‐1, VCAM‐1 total and surface expression) signaling responses and assessed changes in surface N‐glycans and monocyte adhesion.

Significant diversity in responses was evident by disparate changes in ERK1/2 and p65 NF‐κB phosphorylation, which varied up to 5‐fold between different cells and in temporal and magnitude differences in ICAM‐1 and VCAM‐1 expression (maximal VCAM‐1 induction typically being observed by 4 hours, whereas ICAM‐1 expression was increased further at 24 hours relative to 4 hours). N‐glycan profiles both basally and with stimulation were also bed specific, with hypoglycosylated N‐glycans correlating with increased THP‐1 monocyte adhesion. Differences in surface N‐glycan expression tracked with dynamic up‐ or downregulation of α‐mannosidase activity during inflammation.


1. Scott DW, Vallejo MO, Patel RP. Heterogenic endothelial responses to inflammation: role for differential N‐glycosylation and vascular bed of origin. J Am Heart Assoc 2013;2:e000263.​JAHA.113.000263

Published on: August 30, 2013

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