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Verfasst von:Kuk, Hanna [VerfasserIn]   i
 Arnold, Caroline [VerfasserIn]   i
 Hecker, Markus [VerfasserIn]   i
 Korff, Thomas [VerfasserIn]   i
Titel:Magnolol inhibits venous remodeling in mice
Verf.angabe:Hanna Kuk, Caroline Arnold, Ralph Meyer, Markus Hecker & Thomas Korff
E-Jahr:2017
Jahr:19 December 2017
Umfang:13 S.
Fussnoten:Gesehen am 12.04.2018
Titel Quelle:Enthalten in: Scientific reports
Ort Quelle:[London] : Macmillan Publishers Limited, part of Springer Nature, 2011
Jahr Quelle:2017
Band/Heft Quelle:7(2017) Artikel-Nummer 17820, 13 Seiten
ISSN Quelle:2045-2322
Abstract:Due to gravity the venous vasculature in the lower extremities is exposed to elevated pressure levels which may be amplified by obesity or pregnancy. As a consequence, venules dilate and may be slowly transformed into varicose or spider veins. In fact, chronically elevated venous pressure was sufficient to cause the corkscrew-like enlargement of superficial veins in mice. We hypothesized that biomechanical activation of endothelial cells contributes to this process and investigated the inhibitory capacity of Magnolol in this context - a natural compound that features multiple properties counteracting cellular stress. While Magnolol did not influence endothelial capillary sprout formation, it interfered with proliferation, ERK1/2 activity, gelatinase activity as well as baseline production of reactive oxygen species in these cells or murine veins. The anti-oxidative and anti-proliferative capacity of Magnolol was mediated through stimulation of heme oxygenase-1 expression. Finally, local transdermal application of Magnolol attenuated pressure-mediated development of varicose/spider veins in mice and was accompanied by the absence of proliferating and MMP-2 positive endothelial cells. Collectively, our data identified Magnolol as a potent inhibitor of biomechanically evoked endothelial cell activity during pressure-mediated venous remodeling processes which contribute to the development of varicose and spider veins.
DOI:doi:10.1038/s41598-017-17910-0
URL:Kostenfrei: Volltext ; Verlag: http://dx.doi.org/10.1038/s41598-017-17910-0
 Kostenfrei: Volltext: https://www.nature.com/articles/s41598-017-17910-0
 DOI: https://doi.org/10.1038/s41598-017-17910-0
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1571976175
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