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Berti, L. ; Hartwig, S.* ; Irmler, M. ; Raedle, B. ; Siegel-Axel, D. ; Beckers, J. ; Lehr, S.* ; Al-Hasani, H.* ; Häring, H.-U. ; Hrabě de Angelis, M. ; Staiger, H.

Impact of fibroblast growth factor 21 on the secretome of human perivascular preadipocytes and adipocytes: A targeted proteomics approach.

Arch. Physiol. Biochem. 122, 281-288 (2016)
DOI
Open Access Green as soon as Postprint is submitted to ZB.
Context: Perivascular adipose tissue (PVAT) is suggested to impact on vascular cells via humoral factors, possibly contributing to endothelial dysfunction and atherosclerosis. Objective: To address whether the hepatokine fibroblast growth factor (FGF) 21 affects the PVAT secretome. Methods: Human perivascular (pre)adipocytes were subjected to targeted proteomics and whole-genome gene expression analysis. Results: Preadipocytes, as compared to adipocytes, secreted higher amounts of inflammatory cytokines and chemokines. Adipocytes released higher amounts of adipokines [e.g. adipisin, visfatin, dipeptidyl peptidase 4 (DPP4), leptin; p < 0.05, all]. In preadipocytes, omentin 1 release was 1.28-fold increased by FGF-21 (p < 0.05). In adipocytes, FGF-21 reduced chemerin release by 5% and enhanced DPP4 release by 1.15-fold (p < 0.05, both). FGF-21 altered the expression of four secretory genes in preadipocytes and of 18 in adipocytes (p < 0.01, all). Conclusion: The hepatokine FGF-21 exerts secretome-modulating effects in human perivascular (pre)adipocytes establishing a new liver-PVAT-blood vessel axis that possibly contributes to vascular inflammation and atherosclerosis.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Adipokines; Coronary-artery-disease; Adipose-tissue; Insulin-resistance; Metabolic Syndrome; Atherosclerotic Lesion; Dipeptidyl Peptidase-4; Cell-growth; Beta-klotho; Fat-cells; In-vivo
ISSN (print) / ISBN 1381-3455
e-ISSN 1744-4160
Quellenangaben Volume: 122, Issue: 5, Pages: 281-288 Article Number: , Supplement: ,
Publisher Informa Healthcare
Publishing Place Abingdon
Non-patent literature Publications
Reviewing status Peer reviewed