LymphedemaV1, Main, Exploration, bibRecord, 000790

An Important Role of VEGF-C in Promoting Lymphedema Development.

Identifieur interne : 000790 ( Main/Exploration ); précédent : 000789; suivant : 000791

An Important Role of VEGF-C in Promoting Lymphedema Development.

Auteurs : Epameinondas Gousopoulos [Suisse] ; Steven T. Proulx [Suisse] ; Samia B. Bachmann [Suisse] ; Lothar C. Dieterich [Suisse] ; Jeannette Scholl [Suisse] ; Sinem Karaman [Suisse] ; Roberta Bianchi [Suisse] ; Michael Detmar [Suisse]

Source :

The Journal of investigative dermatology [ 1523-1747 ] ; 2017.

RBID : pubmed:28526302

Abstract

Secondary lymphedema is a common complication after cancer treatment, but the pathomechanisms underlying the disease remain unclear. Using a mouse tail lymphedema model, we found an increase in local and systemic levels of the lymphangiogenic factor vascular endothelial growth factor (VEGF)-C and identified CD68(+) macrophages as a cellular source. Surprisingly, overexpression of VEGF-C in a transgenic mouse model led to aggravation of lymphedema with increased immune cell infiltration and vascular leakage compared with wild-type littermates. Conversely, blockage of VEGF-C by overexpression of soluble VEGF receptor-3 reduced edema development, diminishing inflammation and blood vascular leakage. Similar findings were obtained in a hind limb lymph node excision lymphedema model. Flow cytometry analyses and immunofluorescence stainings in lymphedematic tissue showed that VEGF receptor-3 expression was restricted to lymphatic endothelial cells. Our data suggest that endogenous VEGF-C causes blood vascular leakage and fluid influx into the tissue, thus actively contributing to edema formation. These data may provide the basis for future clinical therapeutic approaches.

DOI: 10.1016/j.jid.2017.04.033
PubMed: 28526302

Affiliations:

Suisse

Le document en format XML

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<front><div type="abstract" xml:lang="en">Secondary lymphedema is a common complication after cancer treatment, but the pathomechanisms underlying the disease remain unclear. Using a mouse tail lymphedema model, we found an increase in local and systemic levels of the lymphangiogenic factor vascular endothelial growth factor (VEGF)-C and identified CD68(+) macrophages as a cellular source. Surprisingly, overexpression of VEGF-C in a transgenic mouse model led to aggravation of lymphedema with increased immune cell infiltration and vascular leakage compared with wild-type littermates. Conversely, blockage of VEGF-C by overexpression of soluble VEGF receptor-3 reduced edema development, diminishing inflammation and blood vascular leakage. Similar findings were obtained in a hind limb lymph node excision lymphedema model. Flow cytometry analyses and immunofluorescence stainings in lymphedematic tissue showed that VEGF receptor-3 expression was restricted to lymphatic endothelial cells. Our data suggest that endogenous VEGF-C causes blood vascular leakage and fluid influx into the tissue, thus actively contributing to edema formation. These data may provide the basis for future clinical therapeutic approaches.</div>
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An Important Role of VEGF-C in Promoting Lymphedema Development.

An Important Role of VEGF-C in Promoting Lymphedema Development.

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