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Lymphatic endothelial-cell expressed ACKR3 is dispensable for postnatal lymphangiogenesis and lymphatic drainage function in mice.

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اقرأ على الانترنت اقرأ أكثر حفظ في قائمتي
  • معلومة اضافية
    • المصدر:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: San Francisco, CA : Public Library of Science
    • الموضوع:
      Lymphangiogenesis*; Endothelial Cells/*metabolism ; Lymphatic Vessels/*cytology ; Receptors, CXCR/*metabolism; Animals ; Lymphatic Vessels/physiology ; Mice ; Mice, Inbred C57BL ; Receptors, CXCR/genetics
    • نبذة مختصرة :
      Atypical chemokine receptor ACKR3 (formerly CXCR7) is a scavenging receptor that has recently been implicated in murine lymphatic development. Specifically, ACKR3-deficiency was shown to result in lymphatic hyperplasia and lymphedema, in addition to cardiac hyperplasia and cardiac valve defects leading to embryonic lethality. The lymphatic phenotype was attributed to a lymphatic endothelial cell (LEC)-intrinsic scavenging function of ACKR3 for the vascular peptide hormone adrenomedullin (AM), which is also important during postnatal lymphangiogenesis. In this study, we investigated the expression of ACKR3 in the lymphatic vasculature of adult mice and its function in postnatal lymphatic development and function. We show that ACKR3 is widely expressed in mature lymphatics and that it exerts chemokine-scavenging activity in cultured murine skin-derived LECs. To investigate the role of LEC-expressed ACKR3 in postnatal lymphangiogenesis and function during adulthood, we generated and validated a lymphatic-specific, inducible ACKR3 knockout mouse. Surprisingly, in contrast to the reported involvement of ACKR3 in lymphatic development, our analyses revealed no contribution of LEC-expressed ACKR3 to postnatal lymphangiogenesis, lymphatic morphology and drainage function.
      Competing Interests: The authors have declared that no competing interests exist.
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    • الرقم المعرف:
      0 (Cmkor1 protein, mouse)
      0 (Receptors, CXCR)
    • الموضوع:
      Date Created: 20210415 Date Completed: 20210915 Latest Revision: 20210915
    • الموضوع:
      20250114
    • الرقم المعرف:
      PMC8049313
    • الرقم المعرف:
      10.1371/journal.pone.0249068
    • الرقم المعرف:
      33857173