Stimulation of lymphangiogenesis via VEGFR-3 inhibits chronic skin inflammation
Identifieur interne : 005601 ( Main/Exploration ); précédent : 005600; suivant : 005602Stimulation of lymphangiogenesis via VEGFR-3 inhibits chronic skin inflammation
Auteurs : Reto Huggenberger ; Stefan Ullmann ; Steven T. Proulx ; Bronislaw Pytowski ; Kari Alitalo [Finlande] ; Michael DetmarSource :
- The Journal of Experimental Medicine [ 0022-1007 ] ; 2010.
Abstract
The role of lymphangiogenesis in inflammation has remained unclear. To investigate the role of lymphatic versus blood vasculature in chronic skin inflammation, we inhibited vascular endothelial growth factor (VEGF) receptor (VEGFR) signaling by function-blocking antibodies in the established keratin 14 (K14)–VEGF-A transgenic (Tg) mouse model of chronic cutaneous inflammation. Although treatment with an anti–VEGFR-2 antibody inhibited skin inflammation, epidermal hyperplasia, inflammatory infiltration, and angiogenesis, systemic inhibition of VEGFR-3, surprisingly, increased inflammatory edema formation and inflammatory cell accumulation despite inhibition of lymphangiogenesis. Importantly, chronic Tg delivery of the lymphangiogenic factor VEGF-C to the skin of K14-VEGF-A mice completely inhibited development of chronic skin inflammation, epidermal hyperplasia and abnormal differentiation, and accumulation of CD8 T cells. Similar results were found after Tg delivery of mouse VEGF-D that only activates VEGFR-3 but not VEGFR-2. Moreover, intracutaneous injection of recombinant VEGF-C156S, which only activates VEGFR-3, significantly reduced inflammation. Although lymphatic drainage was inhibited in chronic skin inflammation, it was enhanced by Tg VEGF-C delivery. Together, these results reveal an unanticipated active role of lymphatic vessels in controlling chronic inflammation. Stimulation of functional lymphangiogenesis via VEGFR-3, in addition to antiangiogenic therapy, might therefore serve as a novel strategy to treat chronic inflammatory disorders of the skin and possibly also other organs.
Url:
DOI: 10.1084/jem.20100559
PubMed: 20837699
PubMed Central: 2947063
Affiliations:
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Proulx</name><affiliation><nlm:aff id="aff1"><institution>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland</institution></nlm:aff></affiliation></author><author><name sortKey="Pytowski, Bronislaw" sort="Pytowski, Bronislaw" uniqKey="Pytowski B" first="Bronislaw" last="Pytowski">Bronislaw Pytowski</name><affiliation><nlm:aff id="aff2"><institution>Imclone Systems, New York, NY 10014</institution></nlm:aff></affiliation></author><author><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name><affiliation><nlm:aff id="aff3"><institution>Molecular/Cancer Biology Laboratory, Biomedicum Helsinki, University of Helsinki, FI-00014 Helsinki, Finland</institution></nlm:aff><country>Finlande</country><placeName><settlement type="city">Helsinki</settlement><region type="région" nuts="2">Uusimaa</region></placeName><orgName type="university">Université d'Helsinki</orgName></affiliation></author><author><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><affiliation><nlm:aff id="aff1"><institution>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland</institution></nlm:aff></affiliation></author></analytic><series><title level="j">The Journal of Experimental Medicine</title><idno type="ISSN">0022-1007</idno><idno type="eISSN">1540-9538</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The role of lymphangiogenesis in inflammation has remained unclear. To investigate the role of lymphatic versus blood vasculature in chronic skin inflammation, we inhibited vascular endothelial growth factor (VEGF) receptor (VEGFR) signaling by function-blocking antibodies in the established keratin 14 (K14)–VEGF-A transgenic (Tg) mouse model of chronic cutaneous inflammation. Although treatment with an anti–VEGFR-2 antibody inhibited skin inflammation, epidermal hyperplasia, inflammatory infiltration, and angiogenesis, systemic inhibition of VEGFR-3, surprisingly, increased inflammatory edema formation and inflammatory cell accumulation despite inhibition of lymphangiogenesis. Importantly, chronic Tg delivery of the lymphangiogenic factor VEGF-C to the skin of K14-VEGF-A mice completely inhibited development of chronic skin inflammation, epidermal hyperplasia and abnormal differentiation, and accumulation of CD8 T cells. Similar results were found after Tg delivery of mouse VEGF-D that only activates VEGFR-3 but not VEGFR-2. Moreover, intracutaneous injection of recombinant VEGF-C156S, which only activates VEGFR-3, significantly reduced inflammation. Although lymphatic drainage was inhibited in chronic skin inflammation, it was enhanced by Tg VEGF-C delivery. Together, these results reveal an unanticipated active role of lymphatic vessels in controlling chronic inflammation. Stimulation of functional lymphangiogenesis via VEGFR-3, in addition to antiangiogenic therapy, might therefore serve as a novel strategy to treat chronic inflammatory disorders of the skin and possibly also other organs.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Adams, R H" uniqKey="Adams R">R.H. Adams</name></author><author><name sortKey="Alitalo, K" uniqKey="Alitalo K">K. Alitalo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Angeli, V" uniqKey="Angeli V">V. 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Hu</name></author><author><name sortKey="Kearney, M" uniqKey="Kearney M">M. Kearney</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, Q" uniqKey="Zhang Q">Q. Zhang</name></author><author><name sortKey="Lu, Y" uniqKey="Lu Y">Y. Lu</name></author><author><name sortKey="Proulx, S T" uniqKey="Proulx S">S.T. Proulx</name></author><author><name sortKey="Guo, R" uniqKey="Guo R">R. Guo</name></author><author><name sortKey="Yao, Z" uniqKey="Yao Z">Z. Yao</name></author><author><name sortKey="Schwarz, E M" uniqKey="Schwarz E">E.M. Schwarz</name></author><author><name sortKey="Boyce, B F" uniqKey="Boyce B">B.F. Boyce</name></author><author><name sortKey="Xing, L" uniqKey="Xing L">L. Xing</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Finlande</li></country><region><li>Uusimaa</li></region><settlement><li>Helsinki</li></settlement><orgName><li>Université d'Helsinki</li></orgName></list><tree><noCountry><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><name sortKey="Huggenberger, Reto" sort="Huggenberger, Reto" uniqKey="Huggenberger R" first="Reto" last="Huggenberger">Reto Huggenberger</name><name sortKey="Proulx, Steven T" sort="Proulx, Steven T" uniqKey="Proulx S" first="Steven T." last="Proulx">Steven T. Proulx</name><name sortKey="Pytowski, Bronislaw" sort="Pytowski, Bronislaw" uniqKey="Pytowski B" first="Bronislaw" last="Pytowski">Bronislaw Pytowski</name><name sortKey="Ullmann, Stefan" sort="Ullmann, Stefan" uniqKey="Ullmann S" first="Stefan" last="Ullmann">Stefan Ullmann</name></noCountry><country name="Finlande"><region name="Uusimaa"><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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