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First published online March 18, 2009
doi: 10.1242/10.1242/jcs.041913

Journal of Cell Science 122, 1025-1034 (2009)
Published by The Company of Biologists 2009
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Research Article

Distinct role of PLCβ3 in VEGF-mediated directional migration and vascular sprouting

Resham Bhattacharya1, Junhye Kwon1, Xiujuan Li2, Enfeng Wang1, Sujata Patra1, John Paul Bida1, Zeljko Bajzer1, Lena Claesson-Welsh2 and Debabrata Mukhopadhyay1,*

1 Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
2 Uppsala University, Department of Genetics and Pathology, Rudbeck Laboratory, Dag Hammarskjöldsv. 20, 751 85 Uppsala, Sweden

* Author for correspondence (e-mail: mukhopadhyay.debabrata{at}mayo.edu)

Accepted 3 December 2008

Endothelial cell proliferation and migration is essential to angiogenesis. Typically, proliferation and chemotaxis of endothelial cells is driven by growth factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). VEGF activates phospholipases (PLCs) – specifically PLC{gamma}1 – that are important for tubulogenesis, differentiation and DNA synthesis. However, we show here that VEGF, specifically through VEGFR2, induces phosphorylation of two serine residues on PLCβ3, and this was confirmed in an ex vivo embryoid body model. Knockdown of PLCβ3 in HUVEC cells affects IP3 production, actin reorganization, migration and proliferation; whereas migration is inhibited, proliferation is enhanced. Our data suggest that enhanced proliferation is precipitated by an accelerated cell cycle, and decreased migration by an inability to activate CDC42. Given that PLCβ3 is typically known as an effector of heterotrimeric G-proteins, our data demonstrate a unique crosstalk between the G-protein and receptor tyrosine kinase (RTK) axes and reveal a novel molecular mechanism of VEGF signaling and, thus, angiogenesis.

Key words: Migration, Proliferation, Endothelial signaling, PLCβ3


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VEGF branches out with PLCβ3

JCS 2009 122: 701. [Full Text]  





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