Lymphatic Angiogenesis

During embryonic development, lymphatic growth is initiated after establishment of vascular endothelial cells, a process that may require a transcription factor. Lymphatic channels develop in the arteriolar adventitia after the arteri-oles have become innervated and exhibit active smooth muscle contraction. The lymphatic growth is accompanied by the development of adipose tissue. Lymphatics and lymph nodes in many tissues are surrounded by adipose tissue and control the growth of adipocytes [11].

The homeobox gene transcription factor Prox-1 appears to be required for differentiation of endothelial cells to a lymphatic phenotype [12]. Two peptide lymphangiogenic factors that are members of the VEGF family have been identified to date: VEGF-C and VEGF-D. They have the ability to induce lymphangiogenesis and vasculogenesis. Binding of these growth factors to the vascular endothelial growth factor receptor 3 regulates lymphangiogenesis, in contrast to signaling via the vascular endothelial growth factor receptor-2, which regulates angiogenesis [13]. Overexpression of soluble vascular endothelial growth factor receptor 3 in transgenic mice inhibits lymph channel formation [14]. Other molecules that may play a role in the development of the lymphatic system include angiopoietin-2 and neuropilin-2.

Lymphangiogenesis in wound healing of the skin shows that interstitial fluid channels, detected by fluorescent fluid tracers, form before lymphatic endothelial cell organization. Lymph endothelial cell migration, vascular endothelial growth factor-C expression, and lymphatic capillary network organization are initiated primarily in the direction of lymph flow. These data suggest that lymph channel growth is determined not only by tissue growth factors but also by stresses in the tissue surrounding the lymphatics [15]. Lymphangiogenesis is currently an active research field because of its significance for understanding of lymph edema and metastatic cell dissemination.

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