Research article

Proliferating mesodermal cells in murine embryos exhibiting macrophage and lymphendothelial characteristics

Kerstin Buttler¹ , Taichi Ezaki² and Jörg Wilting^1,3

¹Centre of Anatomy, Department of Anatomy and Cell Biology, University Medicine Goettingen, Goettingen, Germany

²Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo, Japan

³University Medicine Goettingen, Centre of Anatomy, Department of Anatomy and Cell Biology, Kreuzbergring 36, 37075 Goettingen, Germany

author email corresponding author email

BMC Developmental Biology 2008, 8:43doi:10.1186/1471-213X-8-43

Published:	22 April 2008

Abstract

Background

The data on the embryonic origin of lymphatic endothelial cells (LECs) from either deep embryonic veins or mesenchymal (or circulating) lymphangioblasts presently available remain inconsistent. In various vertebrates, markers for LECs are first expressed in specific segments of embryonic veins arguing for a venous origin of lymph vessels. Very recently, studies on the mouse have strongly supported this view. However, in the chick, we have observed a dual origin of LECs from veins and from mesodermal lymphangioblasts. Additionally, in murine embryos we have detected mesenchymal cells that co-express LEC markers and the pan-leukocyte marker CD45. Here, we have characterized the mesoderm of murine embryos with LEC markers Prox1, Lyve-1 and LA102 in combination with macrophage markers CD11b and F4/80.

Results

We observed cells co-expressing both types of markers (e.g. Prox1 – Lyve-1 – F4/80 triple-positive) located in the mesoderm, immediately adjacent to, and within lymph vessels. Our proliferation studies with Ki-67 antibodies showed high proliferative capacities of both the Lyve-1-positive LECs of lymph sacs/lymphatic sprouts and the Lyve-1-positive mesenchymal cells.

Conclusion

Our data argue for a dual origin of LECs in the mouse, although the primary source of embryonic LECs may reside in specific embryonic veins and mesenchymal lymphangioblasts integrated secondarily into lymph vessels. The impact of a dual source of LECs for ontogenetic, phylogenetic and pathological lymphangiogenesis is discussed.