c-Jun N-terminal kinase activation is required for the inhibition of neovascularization by thrombospondin-1 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2001-06

AUTHORS

Benilde Jiménez, Olga V Volpert, Frank Reiher, Lufen Chang, Alberto Muñoz, Michael Karin, Noël Bouck

ABSTRACT

Thrombospondin-1 (TSP-1) is a potent inhibitor of angiogenesis that acts directly on endothelial cells via the CD36 surface receptor molecule to halt their migration, proliferation, and morphogenesis in vitro and to block neovascularization in vivo. Here we show that inhibitory signals elicited by TSP-1 did not alter the ability of inducers of angiogenesis to activate p42 and p44 mitogen-activated protein kinase (MAPK). Rather, TSP-1 induced a rapid and transient activation of c-Jun N-terminal kinases (JNK). JNK activation by TSP-1 required engagement of CD36, as it was blocked by antagonistic CD36 antibodies and stimulated by short anti-angiogenic peptides derived from TSP-1 that act exclusively via CD36. TSP-1 inhibition of corneal neovascularization induced by bFGF was severely impaired in mice null for JNK-1, pointing to a critical role for this stress-activated kinase in the inhibition of neovascularization by TSP-1. More... »

PAGES

1204464

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1204464

DOI

http://dx.doi.org/10.1038/sj.onc.1204464

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044248574

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11423995


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