uu.seUppsala University Publications
Change search
ReferencesLink to record
Permanent link

Direct link
Inhibition of lymphangiogenesis with resulting lymphedema in transgenic mice expressing soluble VEGF receptor-3.
Show others and affiliations
2001 (English)In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 7, no 2Article in journal (Refereed) Published
Abstract [en]

The lymphatic vasculature transports extravasated tissue fluid, macromolecules and cells back into the blood circulation. Recent reports have focused on the molecular mechanisms regulating the lymphatic vessels. Vascular endothelial growth factor (VEGF)-C and VEGF-D have been shown to stimulate lymphangiogenesis and their receptor, VEGFR-3, has been linked to human hereditary lymphedema. Here we show that a soluble form of VEGFR-3 is a potent inhibitor of VEGF-C/VEGF-D signaling, and when expressed in the skin of transgenic mice, it inhibits fetal lymphangiogenesis and induces a regression of already formed lymphatic vessels, though the blood vasculature remains normal. Transgenic mice develop a lymphedema-like phenotype characterized by swelling of feet, edema and dermal fibrosis. They survive the neonatal period in spite of a virtually complete lack of lymphatic vessels in several tissues, and later show regeneration of the lymphatic vasculature, indicating that induction of lymphatic regeneration may also be possible in humans.

Place, publisher, year, edition, pages
2001. Vol. 7, no 2
National Category
Basic Medicine
URN: urn:nbn:se:uu:diva-287175DOI: 10.1038/84651PubMedID: 11175851OAI: oai:DiVA.org:uu-287175DiVA: diva2:922286
Available from: 2016-04-22 Created: 2016-04-22 Last updated: 2016-04-22

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed
In the same journal
Nature Medicine
Basic Medicine

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 6 hits
ReferencesLink to record
Permanent link

Direct link