Table 1.

Phenotypes of transgenic mice lacking or overexpressing Tie receptors and Angiopoietins

Gene	Vascular Phenotype	Lymphatic or haematopoietic Phenotype
Tie1−/−	Die E13.5 onwards. Microvessel haemorrhage, oedema, rupture. Small hearts with endocardial defects 3,4,77 Tie1−/− EC lost from chimaeric WT/Tie1−/− mice 110.
Tie2−/−	Die E9.5 onwards. Poor remodelling, decreased branching, dilated vessels. Fewer EC, rounded EC, lack perivascular cells. Haemorrhage, vessel rupture, endocardial defects 2-5.
Double Tie1−/− /Tie2−/−	Similar Tie2−/− but more severe. Tie1−/− embryo'ssensitive to Tie2 gene dosage 5. Tie1−/−/Tie2−/− EC absent from capillaries of adult chimaeric WT/double knockout mice 5.	Tie1−/−/Tie2−/− cells have reduced capacity to contribute to haematopoiesis in adult, but not foetus 111, Tie1−/− cells can contribute to haematopoiesis 110.
Ang1−/−	Die E12.5. Similar to Tie2−/−. Dilated vessels, EC rounded with poor interaction with matrix/periendothelial cells. Few perivascular cells 1.
Ang1 overexpression	Overexpression in skin increases number & branching of vessels & enlarges vessels 82,112.	Lymphatic hyperplasia in skin of mice overexpressing Ang1 in epidermis97.
Ang2−/−	Die by P14. Failure to remodel & regress hyaloid vasculature, abnormal outgrowth of retinal capillaries & lack of ischaemia- induced neovascularization 113,114.	Defects in lymphangiogenesis - disorganization, hypoplasia in dermal & intestinal lymphatics that can be rescued by Ang1 113.
Ang2 overexpression	Overexpression in EC. Die at E9.5-10.5. Similar to Tie2−/− & Ang1−/−, but more severe. Rounded EC, poor interaction with matrix, endocardial defects 6.