期刊
JOURNAL OF CELL BIOLOGY
卷 168, 期 4, 页码 643-653出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200407060
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资金
- NCI NIH HHS [R37 CA037393, CA45548, CA37393, R01 CA037393, P01 CA045548] Funding Source: Medline
- NHLBI NIH HHS [R01 HL068003, HL68003] Funding Source: Medline
The anti-angiogenic effect of thrombospondin-1 has been shown to be mediated through binding of the type-1 repeat (TSR) domain to the CD36 transmembrane receptor. We now report that the TSR domain can inhibit VEGF-induced migration in human umbilical vein endothelial cells (HUVEC), cells that lack CD36. Moreover, we identified beta(1) integrins as a critical receptor in TSR-mediated inhibition of migration in HUVEC. Using pharmacological inhibitors of downstream VEGF receptor effectors, we found that phosphoinositide 3-kinase (PI3k) was essential for TSR-mediated inhibition of HUVEC migration, but that neither PLCgamma nor Akt was necessary for this response. Furthermore, beta1 integrins were critical for TSR-mediated inhibition of microvascular endothelial cells, cells that express CD36. Together, our results indicate that P, integrins mediate the anti-migratory effects of TSR through a PI3k-dependent mechanism.
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