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. 2011 Dec 20;119(7):1747–1756. doi: 10.1182/blood-2011-09-380709

Figure 1.

Figure 1

Clec1b−/− newborn pups are nonviable and visually distinct from Clec1b+/+ littermates at birth. (A) Blood-filled lymphatic vessels (black arrowhead) in the subcutaneous region of the skin persist at P0 (scale bar = 500 μm). (B) Clec1b−/− newborn pups that feed develop chylous ascites (black arrow) in the abdominal cavity (L indicates lobes of the liver; I, intestine; scale bar = 1 mm). (C) Example of flow cytometric analysis identifying LECs (podoplanin+CD31+) and BECs (podoplanin−CD31+) in the stromal fraction (CD45−Ter119−) of mesenteric vessel preparations from Clec1b+/+ (left) and Clec1b−/− (right) offspring. (D) Ratio of LECs to BECs in preparations of isolated mesenteric vessels (left; **P = .002 by unpaired t test; n = 3 Clec1b+/+; n = 5 Clec1b−/−) and intestine (right; **P = .012 by unpaired t test; n = 3 for each genotype) show significant decreases in P0 Clec1b−/− offspring.