Endothelial-Specific Ablation of ANTXR1, ANTXR2, and MMP14 in Retinal Angiogenesis

In order to determine the angiogenic requirement(s) for ANTXR1, ANTXR2, and MMP14 by removing these genes pairwise specifically in endothelial, pericyte, and smooth muscle cells during sprouting angiogenesis. The mouse retina is a common model used to study sprouting angiogenesis. Vascularization begins when pups are born P(0) and stays confined to a two-dimensional plane. The effects of temporal loss of two loxP flanked alleles during sprouting angiogenesis were evaluated at P(5). Harvested P(5) retina were IHC stained and analyzed for outgrowth, major vessels, branching morphology, & vessel density at the periphery. qPCR analysis of lung and kidney tissue from ANTXR1-/-; R26R-Cre mice validated excision of the ANTXR1 allele. Nine mutant strains were developed using three promotor-driven Cre lines and a combination of two of three alleles. The PDGFRβ-Cre strains lagged slightly due to non-mendelian inheritance of PDGFRβ-Cre. EC specific conditional loss of function mutant mice were studied to elucidate the roles ANTXR1, ANTXR2, and MMP14 play in sprouting angiogenesis and ECM remodeling. No significant phenotypic differences found between endothelial-cell specific conditional loss mice and inter-litter controls.