Lymphatic blood filling in CLEC-2-deficient mouse models

Research output: Contribution to journalArticle


External organisations

  • Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, USA.
  • Institut National de la Santé et de la Recherche Médicale, UMR_S1148, Université Paris Diderot, Sorbonne Paris Cité, Hôpital Bichat, Paris, France
  • Department of Experimental Biomedicine; University Hospital, University of Würzburg; Würzburg Germany


C-type lectin-like receptor 2 (CLEC-2) is considered as a potential drug target in settings of wound healing, inflammation, and infection. A potential barrier to this is evidence that CLEC-2 and its ligand podoplanin play a critical role in preventing lymphatic vessel blood filling in mice throughout life. In this study, this aspect of CLEC-2/podoplanin function is investigated in more detail using new and established mouse models of CLEC-2 and podoplanin deficiency, and models of acute and chronic vascular remodeling. We report that CLEC-2 expression on platelets is not required to maintain a barrier between the blood and lymphatic systems in unchallenged mice, post-development. However, under certain conditions of chronic vascular remodeling, such as during tumorigenesis, deficiency in CLEC-2 can lead to lymphatic vessel blood filling. These data provide a new understanding of the function of CLEC-2 in adult mice and confirm the essential nature of CLEC-2-driven platelet activation in vascular developmental programs. This work expands our understanding of how lymphatic blood filling is prevented by CLEC-2-dependent platelet function and provides a context for the development of safe targeting strategies for CLEC-2 and podoplanin.


Original languageEnglish
Early online date4 Mar 2020
Publication statusE-pub ahead of print - 4 Mar 2020


  • Blood-lymphatic separation, CLEC-2, platelets, podoplanin

ASJC Scopus subject areas