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Article: MT1-MMP sheds LYVE-1 on lymphatic endothelial cells and suppresses VEGF-C production to inhibit lymphangiogenesis

TitleMT1-MMP sheds LYVE-1 on lymphatic endothelial cells and suppresses VEGF-C production to inhibit lymphangiogenesis
Authors
Issue Date2016
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ncomms/index.html
Citation
Nature Communications, 2016, v. 7, p. 10824:1-17 How to Cite?
AbstractLymphangiogensis is involved in various pathological conditions, such as arthritis and cancer metastasis. Although many factors have been identified to stimulate lymphatic vessel growth, little is known about lymphangiogenesis inhibitors. Here we report that membrane type 1-matrix metalloproteinase (MT1-MMP) is an endogenous suppressor of lymphatic vessel growth. MT1-MMP-deficient mice exhibit spontaneous corneal lymphangiogenesis without concomitant changes in angiogenesis. Mice lacking MT1-MMP in either lymphatic endothelial cells or macrophages recapitulate corneal lymphangiogenic phenotypes observed in Mmp14−/− mice, suggesting that the spontaneous lymphangiogenesis is both lymphatic endothelial cells autonomous and macrophage associated. Mechanistically, MT1-MMP directly cleaves LYVE-1 on lymphatic endothelial cells to inhibit LYVE-1-mediated lymphangiogenic responses. In addition, MT1-MMP-mediated PI3Kδ signalling restrains the production of VEGF-C from prolymphangiogenic macrophages through repressing the activation of NF-κB signalling. Thus, we identify MT1-MMP as an endogenous inhibitor of physiological lymphangiogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/234390
ISSN
2015 Impact Factor: 11.329
2015 SCImago Journal Rankings: 6.539

 

DC FieldValueLanguage
dc.contributor.authorWong, HLX-
dc.contributor.authorJin, G-
dc.contributor.authorCao, R-
dc.contributor.authorZhang, S-
dc.contributor.authorCao, Y-
dc.contributor.authorZhou, Z-
dc.date.accessioned2016-10-14T13:46:32Z-
dc.date.available2016-10-14T13:46:32Z-
dc.date.issued2016-
dc.identifier.citationNature Communications, 2016, v. 7, p. 10824:1-17-
dc.identifier.issn2041-1723-
dc.identifier.urihttp://hdl.handle.net/10722/234390-
dc.description.abstractLymphangiogensis is involved in various pathological conditions, such as arthritis and cancer metastasis. Although many factors have been identified to stimulate lymphatic vessel growth, little is known about lymphangiogenesis inhibitors. Here we report that membrane type 1-matrix metalloproteinase (MT1-MMP) is an endogenous suppressor of lymphatic vessel growth. MT1-MMP-deficient mice exhibit spontaneous corneal lymphangiogenesis without concomitant changes in angiogenesis. Mice lacking MT1-MMP in either lymphatic endothelial cells or macrophages recapitulate corneal lymphangiogenic phenotypes observed in Mmp14−/− mice, suggesting that the spontaneous lymphangiogenesis is both lymphatic endothelial cells autonomous and macrophage associated. Mechanistically, MT1-MMP directly cleaves LYVE-1 on lymphatic endothelial cells to inhibit LYVE-1-mediated lymphangiogenic responses. In addition, MT1-MMP-mediated PI3Kδ signalling restrains the production of VEGF-C from prolymphangiogenic macrophages through repressing the activation of NF-κB signalling. Thus, we identify MT1-MMP as an endogenous inhibitor of physiological lymphangiogenesis.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ncomms/index.html-
dc.relation.ispartofNature Communications-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleMT1-MMP sheds LYVE-1 on lymphatic endothelial cells and suppresses VEGF-C production to inhibit lymphangiogenesis-
dc.typeArticle-
dc.identifier.emailWong, HLX: wohole@hku.hk-
dc.identifier.emailZhang, S: mistyzs@HKUCC-COM.hku.hk-
dc.identifier.emailZhou, Z: zhongjun@hku.hk-
dc.identifier.authorityZhou, Z=rp00503-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/ncomms10824-
dc.identifier.hkuros268041-
dc.identifier.volume7-
dc.identifier.spage10824:1-
dc.identifier.epage17-
dc.publisher.placeUnited Kingdom-

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