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Loss of p53 compensates for alpha(v)-integrin function in retinal neovascularization
Södertörns högskola, Avdelning Naturvetenskap.
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2002 (Engelska)Ingår i: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 277, nr 16, s. 13371-13374Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

alpha(v)-Integrin antagonists block neovascularization in various species, whereas 20% of alpha(v)-integrin null mice are born with many normal looking blood vessels. Given that blockade of alpha(v)-integrins during angiogenesis induces p53 activity, we utilized p53 null mice to elucidate whether loss of p53 can compensate for av-integrin function in neovascularization of the retina. Murine retinal vascularization was inhibited by systemic administration of an alpha(v)-integrin antagonist. In contrast, mice lacking p53 were refractory to this treatment, indicating that neovascularization in normal mice depends on alpha(v)-integrin-mediated suppression of p53. Blockade of alpha(v)-integrins during neovascularization resulted in an induction of p21(CIP1) in wild type and, surprisingly, in p53 null retinas, indicating that alpha(v)-integrin ligation regulates p21(CIP1) levels in a p53-independent manner. In conclusion, we demonstrate for the first time an in vivo intracellular mechanism for compensation of integrin function and that p53 and alpha(v)-integrins act in concert during retinal neovascularization.

Ort, förlag, år, upplaga, sidor
2002. Vol. 277, nr 16, s. 13371-13374
Nationell ämneskategori
Biokemi och molekylärbiologi
Identifikatorer
URN: urn:nbn:se:sh:diva-15806DOI: 10.1074/jbc.C200044200ISI: 000175096000004PubMedID: 11856728OAI: oai:DiVA.org:sh-15806DiVA, id: diva2:508482
Tillgänglig från: 2012-03-08 Skapad: 2012-03-07 Senast uppdaterad: 2017-12-07Bibliografiskt granskad

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