2026-06-30T02:00:50Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/64992024-09-27T07:56:44Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Theodorou, Kosta
author
van der Vorst, Emiel P. C.
author
Gijbels, Marion J.
author
Wolfs, Ine M. J.
author
Jeurissen, Mike
author
Theelen, Thomas L.
author
Sluimer, Judith C.
author
Wijnands, Erwin
author
Cleutjens, Jack P.
author
Li, Yu
author
Jansen, Yvonne
author
Weber, Christian
author
Ludwig, Andreas
author
Bentzon, Jacob F
author
Bartsch, Joerg W.
author
Biessen, Erik A. L.
author
Donners, Marjo M. P. C.
funder
CARIM PhD-award
funder
Deutsche Forschungsgemeinschaft (Alemania)
funder
Alexander von Humboldt Foundation
2018-10-19T08:00:43Z
2018-10-19T08:00:43Z
2017
Sci Rep. 2017; 7(1):11670
10.1038/s41598-017-10549-x
2045-2322
Scientific Reports
28916789
http://hdl.handle.net/20.500.12105/6499
Although A Disintegrin And Metalloproteinase 8 (ADAM8) is not crucial
for tissue development and homeostasis, it has been implicated in
various inflammatory diseases by regulating processes like immune cell
recruitment and activation. ADAM8 expression has been associated with
human atherosclerosis development and myocardial infarction, however a
causal role of ADAM8 in atherosclerosis has not been investigated thus
far. In this study, we examined the expression of ADAM8 in early and
progressed human atherosclerotic lesions, in which ADAM8 was
significantly upregulated in vulnerable lesions. In addition, ADAM8
expression was most prominent in the shoulder region of human
atherosclerotic lesions, characterized by the abundance of foam cells.
In mice, Adam8 was highly expressed in circulating neutrophils and in
macrophages. Moreover, ADAM8 deficient mouse macrophages displayed
reduced secretion of inflammatory mediators. Remarkably, however,
neither hematopoietic nor whole-body ADAM8 deficiency in mice affected
atherosclerotic lesion size. Additionally, except for an increase in
granulocyte content in plaques of ADAM8 deficient mice, lesion
morphology was unaffected. Taken together, whole body and hematopoietic
ADAM8 does not contribute to advanced atherosclerotic plaque
development, at least in female mice, although its expression might
still be valuable as a diagnostic/ prognostic biomarker to distinguish
between stable and unstable lesions.
eng
METALLOPROTEASE-DISINTEGRIN ADAM8
TUMOR-NECROSIS-FACTOR
MYOCARDIAL-INFARCTION
TNF-ALPHA
EXPRESSION ANALYSIS
PERIPHERAL-BLOOD
DENDRITIC CELLS
TRANSGENIC MICE
IMMUNE-SYSTEM
MACROPHAGES
Whole body and hematopoietic ADAM8 deficiency does not influence
advanced atherosclerotic lesion development, despite its association
with human plaque progression
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WholeBodyHematopoieticADAM8_2017.pdf.txt
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