Title
The dipeptidyl peptidases 4, 8, and 9 in mouse monocytes and macrophages : DPP8/9 inhibition attenuates M1 macrophage activation in mice The dipeptidyl peptidases 4, 8, and 9 in mouse monocytes and macrophages : DPP8/9 inhibition attenuates M1 macrophage activation in mice
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences. Pharmacy
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Publication type
article
Publication
New York ,
Subject
Biology
Pharmacology. Therapy
Veterinary medicine
Human medicine
Source (journal)
Inflammation. - New York
Volume/pages
39(2016) :1 , p. 413-424
ISSN
0360-3997
ISI
000370083500046
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
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.
E-info
https://repository.uantwerpen.be/docman/iruaauth/ca1e56/128186.pdf
Full text (open access)
https://repository.uantwerpen.be/docman/irua/71c2dc/128186.pdf
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