Publication
Title
The dipeptidyl peptidases 4, 8, and 9 in mouse monocytes and macrophages : DPP8/9 inhibition attenuates M1 macrophage activation in mice
Author
Abstract
Atherosclerosis remains the leading cause of death in Western countries. Dipeptidyl peptidase (DPP) 4 has emerged as a novel target for the prevention and treatment of atherosclerosis. Family members DPP8 and 9 are abundantly present in macrophage-rich regions of atherosclerotic plaques, and DPP9 inhibition attenuates activation of human M1 macrophages in vitro. Studying this family in a mouse model for atherosclerosis would greatly advance our knowledge regarding their potential as therapeutic targets. We found that DPP4 is downregulated during mouse monocyte-to-macrophage differentiation. DPP8 and 9 expression seems relatively low in mouse monocytes and macrophages. Viability of primary mouse macrophages is unaffected by DPP4 or DPP8/9 inhibition. Importantly, DPP8/9 inhibition attenuates macrophage activation as IL-6 secretion is significantly decreased. Mouse macrophages respond similarly to DPP inhibition, compared to human macrophages. This shows that the mouse could become a valid model species for the study of DPPs as therapeutic targets in atherosclerosis.
Language
English
Source (journal)
Inflammation. - New York
Publication
New York : 2016
ISSN
0360-3997
DOI
10.1007/S10753-015-0263-5
Volume/pages
39 :1 (2016) , p. 413-424
ISI
000370083500046
Pubmed ID
26454447
Full text (Publisher's DOI)
Full text (open access)
Full text (publisher's version - intranet only)
UAntwerpen
Faculty/Department
Research group
Project info
INFLA-MED - Fundamental research in the pathophysiological processes of inflammatory diseases.
Expression and role of dipeptidyl peptidases and related peptidases in acute lung injury.
Publication type
Subject
Affiliation
Publications with a UAntwerp address
External links
Web of Science
Record
Identifier
Creation 15.10.2015
Last edited 28.01.2024
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