http://atvb.ahajournals.org/content/34/9/1809.extract?etoc
+ Author Affiliations
- Correspondence to Aldons J. Lusis, PhD, Division of Cardiology, Department of Medicine, A2-237 CHS, University of California, Los Angeles, Los Angeles, CA 90095. E-mail jlusis@mednet.ucla.edu
In the current issue of ATVB, Shang et al provide compelling evidence for the involvement of LIM domain binding 2 (LDB2) in the transendothelial migration
of monocytes in atherosclerosis.1 The article is also of interest because of the systems analyses that led to its identification as a strong candidate.
See accompanying article on page 2068
LDB2 was identified earlier as a key driver of atherosclerosis based on studies of gene expression profiles of tissues obtained
from patients.2
Using samples from the Stockholm Atherosclerosis Gene Expression
(STAGE) study, the authors profiled gene expression of 5
atherosclerosis-relevant tissues from 114
patients undergoing coronary artery bypass grafting. The tissues
collected were
distal internal mammary artery, wall of the
ascending aorta at the aortic root, anterior hepatic edge, skeletal
muscle, and
visceral fat. A total of 278 gene expression
profiles were used in a coupled 2-way clustering analysis3
to identify 60 gene subnetworks in these tissues. Two of the gene
clusters, one in atherosclerotic arterial wall (49 genes)
and the other in visceral fat (59 genes),
segregated the patients according to the extent of atherosclerosis as
measured by
quantitative coronary angiography. The authors
further validated their findings using expression data obtained from
carotid
lesions isolated from patients undergoing
carotid stenosis surgery. Clustering of data identified 8 gene
subnetworks in carotid
lesions, one of which segregated the patients
according to the extent of atherosclerosis as measured by
ultrasound-measured
intima-media thickness. This cluster
significantly overlapped with the 2 previously identified clusters from …
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