1,721,055 research outputs found

    SIP1/ZEB2 Targeting by the Nitric Oxide-dependent miR200 Family is Important for Early Mesodermic/Cardiovascular Commitment of Mouse Embryonic Stem Cells

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    Taken altogether our data identifies the mir200 family as responsive to NO treatment and provide evidences about the role of Sip1/ZEB2 in the regulation of the nitric oxide-dependent early cardiovascular ES differentiation

    In vitro and in vivo models to study chemokine regulation of angiogenesis

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    Angiogenesis is defined as the generation of new blood vessels from preexisting ones. Physiologic angiogenesis is a controlled and fundamental process during embryonic development, being rare in the adult and limited to conditions such as wound healing and menstrual cycle. If regulation of the process is lost, persistent angiogenesis may occur and contribute to pathologic states such as cancer, rheumatoid arthritis, and diabetes mellitus

    E1A stimulates FGF-2 release promoting differentiation of primary endothelial cells

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    Basic Fibroblast Growth Factor (FGF-2) is a growth and survival factor and represents one of the most potent differentiation agents of vascular system. In the present study we describe that adenoviral oncoprotein E1A regulates FGF-2 production and determines the acquisition of a pro-angiogenic phenotype in primary bovine aortic endothelial cells (BAEC). Following their transfection, wild type E1A proteins 12S and 13S (wtE1A) stimulated BAEC to differentiate on reconstituted basement membrane matrix (Matrigel). This outcome was paralleled by invasion and migration enhancement in wtE1A-transfected cells. This stimulating effect was absent with the E1A mutant dl646N. Accordingly, zymography and RT - PCR analyses showed that matrix metalloproteinase-9 protein- and mRNA-levels increased following wtE1A transfection. Interestingly, wtE1A-transfected BAEC showed FGF-2 mRNA- and protein-levels higher than controls. Further, FGF-2 neutralization reduced the amount of MMP-9 released in the supernatant of E1A-transfected cells and strongly inhibited BAEC differentiation, thus suggesting that wtE1A activates BAEC by a mechanism, at least partially, dependent on a FGF-2 autocrine/paracrine loop
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