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Class 3 semaphorins negatively regulate dermal lymphatic network formation.

Yutaka Uchida1, Jennifer M James1, Fumikazu Suto2

  • 1Laboratory of Stem Cell and Neuro-Vascular Biology, Genetics and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 10/6C103, 10 Center Drive, Bethesda, MD 20892, USA.

Biology Open
|August 31, 2015
PubMed
Summary
This summary is machine-generated.

Class 3 semaphorins (SEMA3F and SEMA3G) negatively regulate lymphatic endothelial cell growth and sprouting, controlling dermal lymphatic network formation. This study reveals their crucial role in lymphangiogenesis.

Keywords:
Dermal lymphangiogenesisLEC growthLEC sproutingNRP2SEMA3s

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Area of Science:

  • Developmental Biology
  • Vascular Biology
  • Cell Biology

Background:

  • Lymphatic vascular network development is crucial for organ function and homeostasis.
  • Class 3 semaphorins (SEMA3s) are known regulators of neuronal development.
  • The role of SEMA3s in lymphatic development was previously unclear.

Purpose of the Study:

  • To investigate the role of SEMA3F and SEMA3G in dermal lymphatic network formation.
  • To identify the receptors and signaling pathways involved in SEMA3-mediated regulation of lymphatic endothelial cells (LECs).

Main Methods:

  • In vitro studies using human dermal LECs to assess the effects of SEMA3F and SEMA3G on VEGFC-mediated responses.
  • In vivo studies using genetically modified mice (Sema3f;Sema3g double mutants, Nrp2 mutants, PlexinA1/A2 mutants) to analyze dermal lymphatic development.
  • Immunohistochemistry to examine the expression patterns of SEMA3s and their receptors in developing mouse skin.

Main Results:

  • SEMA3F and SEMA3G inhibit VEGFC-induced LEC sprouting and proliferation in vitro.
  • SEMA3F and SEMA3G act as negative regulators of LEC growth and dermal lymphatic network formation in vivo.
  • NRP2 functions as a receptor for SEMA3F and SEMA3G, mediating their inhibitory effects.
  • Reciprocal phenotypes in lymphatic branching between Sema3f;Sema3g mutants and Nrp2 mutants suggest a complex role for NRP2.

Conclusions:

  • SEMA3F and SEMA3G are essential negative regulators of dermal lymphangiogenesis.
  • NRP2 plays a dual role in LEC regulation, acting as a receptor for both inhibitory SEMA3s and potentially growth-promoting factors like VEGFC.
  • PlexinA1 and PlexinA2 are downstream effectors of SEMA3 signaling in LECs.