p38 MAP kinase negatively regulates endothelial cell survival, proliferation, and differentiation in FGF-2-stimulated angiogenesis

doi:10.1083/jcb.200103096

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Published 7 January 2002. doi:10.1083/jcb.200103096

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© The Rockefeller University Press, 0021-9525/2002/1/149 $5.00
The Journal of Cell Biology, Volume 156, Number 1, January 7, 2002 149-160

Article

p38 MAP kinase negatively regulates endothelial cell survival, proliferation, and differentiation in FGF-2–stimulated angiogenesis

Taro Matsumoto¹, Ingela Turesson², Majlis Book², Pär Gerwins¹ and Lena Claesson-Welsh¹

¹ Department of Genetics and Pathology, Radiology, and Clinical Immunology, Rudbeck Laboratory, Uppsala University, Uppsala, S-751 85, Sweden
² Department of Oncology, Radiology, and Clinical Immunology, Rudbeck Laboratory, Uppsala University, Uppsala, S-751 85, Sweden

Address correspondence to Lena Claesson-Welsh, Dept. of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, S-751 85, Sweden. Tel.: 46-18-471-4363. Fax: 46-18-55-89-31. E-mail: lena.welsh{at}genpat.uu.se

The p38 mitogen–activated protein kinase (p38) is activatedin response to environmental stress and inflammatory cytokines.Although several growth factors, including fibroblast growthfactor (FGF)-2, mediate activation of p38, the consequencesfor growth factor–dependent cellular functions have notbeen well defined. We investigated the role of p38 activationin FGF-2–induced angiogenesis. In collagen gel cultures,bovine capillary endothelial cells formed tubular growth-arrestedstructures in response to FGF-2. In these collagen gel cultures,p38 activation was induced more potently by FGF-2 treatmentcompared with that in proliferating cultures. Treatment withthe p38 inhibitor SB202190 enhanced FGF-2–induced tubularmorphogenesis by decreasing apoptosis, increasing DNA synthesisand cell proliferation, and enhancing the kinetics of cell differentiationincluding increased expression of the Notch ligand Jagged1.Overexpression of dominant negative mutants of the p38-activatingkinases MKK3 and MKK6 also supported FGF-2–induced tubularmorphogenesis. Sustained activation of p38 by FGF-2 was identifiedin vascular endothelial cells in vivo in the chick chorioallantoicmembrane (CAM). SB202190 treatment enhanced FGF-2–inducedneovascularization in the CAM, but the vessels displayed abnormalfeatures indicative of hyperplasia of endothelial cells. Theseresults implicate p38 in organization of new vessels and suggestthat p38 is an essential regulator of FGF-2–driven angiogenesis.

Key Words: p38 mitogen–activated protein kinase; differentiation; angiogenesis; fibroblast growth factor; vascular endothelial growth factor

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