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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:604-605
doi: 10.1161/ATVBAHA.108.162032
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:604.)
© 2008 American Heart Association, Inc.


Editorials

VEGFR1 for Lymphangiogenesis

An Alternative Signaling Pathway?

Yasufumi Sato

From the Department of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University, Japan.

Correspondence to Yasufumi Sato, Department of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan. E-mail y-sato@idac. tohoku.ac.jp


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

The lymphatic vascular system is a conduit for interstitial fluid extravasated from blood vessels and also plays important roles in maintaining immune responses, lipid uptake, and tissue homeostasis. In recent years, much attention has been given to lymphangiogenesis, a formation of new lymphatic vessels, because lymphangiogenesis has been shown to be involved in lymph node metastasis of tumors.1

See accompanying article on page 658

The development of blood and lymphatic vascular systems is primarily regulated by vascular endothelial growth factor (VEGF) family members. This family consists of 5 members: VEGF-A, VEGF-B, VEGF-C, VEGF-D, and placenta growth factor (PlGF). There are 3 members of VEGF receptor (VEGFR) tyrosine kinases: VEGFR1, VEGFR2, and VEGFR3. Members of the VEGF family show different affinities for these receptors. VEGFR1 is able to bind VEGF-A, VEGF-B, and PlGF. VEGFR2 is activated primarily by VEGF-A, but cleaved forms of VEGF-C and VEGF-D may also activate this receptor. VEGFR3 is activated by VEGF-C and VEGF-D. Vascular endothelial cells (ECs) express VEGFR1 and VEGFR2, whereas lymphatic ECs express VEGFR2 and VEGFR3 in the adult. The most important molecule in the VEGF family that controls angiogenesis is VEGF-A, and VEGFR2 is the major mediator of VEGF-A driven responses in vascular ECs. VEGFR1, on the other hand, has a higher affinity for VEGF-A but weaker tyrosine kinase activity. Thus, VEGFR1 on vascular ECs may act as a counter-regulator of VEGFR2. VEGFR1 is also expressed by monocytes/macrophages and hematopoietic stem cells, and in those cases, VEGFR1 transduces signal for the migration of . . . [Full Text of this Article]


Related Article:

VEGFR1 Tyrosine Kinase Signaling Promotes Lymphangiogenesis as Well as Angiogenesis Indirectly via Macrophage Recruitment
Masato Murakami, Yujuan Zheng, Masanori Hirashima, Toshio Suda, Yohei Morita, Jun Ooehara, Hideo Ema, Guo-Hua Fong, and Masabumi Shibuya
Arterioscler Thromb Vasc Biol 2008 28: 658-664. [Abstract] [Full Text] [PDF]