LymphedemaV1, PubMed, Corpus, bibRecord, 000194

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

Identifieur interne : 000194 ( PubMed/Corpus ); précédent : 000193; suivant : 000195

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

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

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

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<author><name sortKey="Proulx, Steven T" sort="Proulx, Steven T" uniqKey="Proulx S" first="Steven T" last="Proulx">Steven T. Proulx</name>
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<author><name sortKey="Bachmann, Samia B" sort="Bachmann, Samia B" uniqKey="Bachmann S" first="Samia B" last="Bachmann">Samia B. Bachmann</name>
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<author><name sortKey="Dieterich, Lothar C" sort="Dieterich, Lothar C" uniqKey="Dieterich L" first="Lothar C" last="Dieterich">Lothar C. Dieterich</name>
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<author><name sortKey="Karaman, Sinem" sort="Karaman, Sinem" uniqKey="Karaman S" first="Sinem" last="Karaman">Sinem Karaman</name>
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<author><name sortKey="Bianchi, Roberta" sort="Bianchi, Roberta" uniqKey="Bianchi R" first="Roberta" last="Bianchi">Roberta Bianchi</name>
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<author><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name>
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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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<Abstract><AbstractText>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.</AbstractText>
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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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