VEGF in the Crosstalk between Human Adipocytes and Smooth Muscle Cells: Depot-Specific Release from Visceral and Perivascular Adipose TissueReportar como inadecuado

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Mediators of InflammationVolume 2013 2013, Article ID 982458, 10 pages

Research Article

Paul-Langerhans-Group, Integrative Physiology, German Diabetes Center, Auf-m Hennekamp 65, 40225 Düsseldorf, Germany

Department of General-, Visceral-, and Pediatric Surgery, Heinrich-Heine-University and University Hospital Düsseldorf, 40225 Düsseldorf, Germany

Signal Transduction, Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, 40225 Düsseldorf, Germany

Department of Endocrinology, Ghent University Hospital, 9000 Ghent, Belgium

Department of Cardiovascular Surgery, Düsseldorf University Hospital, 40225 Düsseldorf, Germany

Received 28 February 2013; Revised 10 June 2013; Accepted 10 June 2013

Academic Editor: Daniel Konrad

Copyright © 2013 Raphaela Schlich et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Adipose tissue secrets adipokines and fatty acids, which may contribute to obesity-associated vascular dysfunction and cardiovascular risk. This study investigated which factors are responsible for the synergistic effect of adipokine and oleic acid- OA- induced proliferation of human vascular smooth muscle cells VSMC. Adipocyte-conditioned medium CM from human adipocytes induces proliferation of VSMC in correlation to its vascular endothelial growth factor VEGF content. CM increases VEGF-receptor VEGF-R 1 and 2 expression and VEGF secretion of VSMC, while OA only stimulates VEGF secretion. VEGF neutralization abrogates CM- and OA-induced proliferation and considerably reduces proliferation induced by CM and OA in combination. VEGF release is higher from visceral adipose tissue VAT of obese subjects compared to subcutaneous adipose tissue SAT and VAT from lean controls. Furthermore, VEGF release from VAT correlates with its proliferative effect. Perivascular adipose tissue PAT from type 2 diabetic patients releases significantly higher amounts of VEGF and induces stronger proliferation of VSMC as compared to SAT and SAT-PAT of nondiabetics. In conclusion, VEGF is mediating CM-induced proliferation of VSMC. As this adipokine is released in high amounts from VAT of obese patients and PAT of diabetic patients, VEGF might link adipose tissue inflammation to increased VSMC proliferation.

Autor: Raphaela Schlich, Miriam Willems, Sabrina Greulich, Florian Ruppe, Wolfram Trudo Knoefel, D. Margriet Ouwens, Bujar Maxhera,



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