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Bcl‐2 Regulates Endothelial Cell Migration and Capillary Morphogenesis
Author(s) -
Sorenson Christine M,
Kondo Shuji,
Tang Yixin,
Sheibani Nader
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.746.1
Subject(s) - microbiology and biotechnology , angiogenesis , retinal , morphogenesis , biology , retina , matrigel , endothelial stem cell , pericyte , chemistry , cancer research , neuroscience , biochemistry , in vitro , gene
Apoptosis plays a critical role during development and in the maintenance of multicellular organisms. B cell leukemia lymphoma 2 (bcl‐2) protects endothelial cells (EC) from apoptosis in response to a variety of stimuli. Previous work from this laboratory demonstrated attenuation of postnatal retinal vascular development and retinal neovascularization during oxygen‐induced ischemic retinopathy in bcl‐2 deficient (bcl‐2 −/−) mice. How bcl‐2 affects EC function during these processes require further investigation. To gain further insight into the functions of bcl‐2 in the endothelium we isolated retinal EC from bcl‐2 +/+ and bcl‐2 −/− mice. Retinal EC lacking bcl‐2 demonstrated reduced cell migration, reduced tenascin‐C expression, and reduced adhesion to vitronectin and fibronectin. The bcl‐2 −/− retinal EC also failed to undergo capillary morphogenesis in Matrigel. In addition, using an ex vivo angiogenesis assay we observed reduced sprouting from aortic rings grown in culture from bcl‐2 −/− mice compared to bcl‐2 +/+ mice. Furthermore, re‐expression of bcl‐2 was sufficient to restore migration and capillary morphogenesis defects observed in bcl‐2−/− retinal EC. Thus, bcl‐2‐mediated functions play an important role in EC migration and capillary morphogenesis during retinal vascular development and angiogenesis.