Foxc2 is expressed in developing lymphatic vessels and other tissues associated with lymphedema-distichiasis syndrome

Susan L. Dagenais, Rebecca L. Hartsough, Robert P. Erickson, Marlys H Witte, Matthew G. Butler, Thomas W. Glover

Research output: Contribution to journalArticle

73 Scopus citations


The molecular events involved in lymphatic development are poorly understood. Hence, the genes responsible for hereditary lymphedema are of great interest due to the potential for providing insights into the mechanisms of lymphatic development, the diagnosis, prevention and treatment of lymphedema, and lymphangiogenesis during tumor growth. Mutations in the FOXC2 transcription factor cause a major form of hereditary lymphedema, the lymphedema-distichiasis syndrome. We have conducted a study of Foxc2 expression during mouse development using immunohistochemistry, and examined its expression in lymphatics compared to its paralog Foxc1 and to Vegfr-3, Prox1 and other lymphatic and blood vascular proteins. We have found that Foxc2 is expressed in lymphatic primordia, jugular lymph sacs, lymphatic collectors and capillaries, as well as in podocytes, developing eyelids and other tissues associated with abnormalities in lymphedema-distichiasis syndrome.

Original languageEnglish (US)
Pages (from-to)611-619
Number of pages9
JournalGene Expression Patterns
Issue number6
Publication statusPublished - Oct 2004



  • Distichiasis
  • Forkhead
  • Foxc1
  • Foxc2
  • Lymphangiogenesis
  • Lymphatic
  • Lymphedema
  • Lymphedema-distichiasis
  • LYVE-1
  • Mfh-1
  • Mfh1
  • Nephrin
  • Podocytes
  • Podoplanin
  • Prox1
  • Vegfr-3
  • Winged-helix

ASJC Scopus subject areas

  • Genetics
  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Developmental Neuroscience

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