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(Circulation Research. 2007;101:642.)
© 2007 American Heart Association, Inc.

Editorials

Sympathetic Control of VEGF Angiogenic Signaling

Dual Regulations by ₂-Adrenoceptor Activation?

Yuichi Hattori, Seiji Yamamoto, Naoyuki Matsuda

From the Department of Molecular and Medical Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Japan.

Correspondence to Yuichi Hattori, Department of Molecular and Medical Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan. E-mail yhattori@med.u-toyama.ac.jp

See related article, pages 682–691

Key Words: adrenergic receptors • angiogenesis • vascular endothelial growth factor • vascular endothelial growth factor receptors

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

It is now accepted that vascular endothelial growth factor (VEGF), a dimeric 46-kDa heparin-binding glycoprotein, is one of the most important vasculogenic and angiogenic factors reported to date. VEGF acts as a potent and specific mitogen for vascular endothelial cells in vitro and possesses a signal sequence which allows it to be secreted.¹ Furthermore, numerous studies in vivo have shown that expression of VEGF and its receptors is upregulated during angiogenesis under physiological and pathological processes, such as development of the embryo,^2–4 estrous cycle,⁵ tumor growth,^6,7 and wound healing.⁸ Thus, VEGF plays an important role in the formation of new vessels from existing ones and the microvascular remodeling which involves structural alterations—usually enlargement—of arterioles, capillaries, or venules, in inflammatory or neoplastic diseases.

Different mechanisms appear to participate in the regulation of VEGF mRNA expression. It is well known that low oxygen tension is a strong inducer of VEGF mRNA expression in a variety of cells.^6,9 Besides hypoxia-sensitive elements, the VEGF promoter region contains potential binding sites for the transcription factors AP-1, AP-2, and SP-1.¹⁰ Consistent with this fact, cAMP analogues and phorbol esters have been shown to upregulate VEGF mRNA in rat aortic smooth muscle cells,¹¹ NIH 3T3 cells,¹² or ovarian bovine granulosa cells,¹³ suggesting that VEGF expression is controlled by protein kinase A (PKA)- and protein kinase C (PKC)-mediated signals. Very interestingly, norepinephrine has been demonstrated to increase VEGF expression in murine brown adipocytes.^14–16 Stimulation of ß-adrenoceptors with norepinephrine activates adenylate cyclase via G_s regulatory proteins, resulting in an . . . [Full Text of this Article]

Related Article:

Upregulation of Soluble Vascular Endothelial Growth Factor Receptor 1 Contributes to Angiogenesis Defects in the Placenta of _2B-Adrenoceptor–Deficient Mice

Verena Muthig, Ralf Gilsbach, Miriam Haubold, Melanie Philipp, Tomi Ivacevic, Manfred Gessler, and Lutz Hein
Circ. Res. 2007 101: 682-691. [Abstract] [Full Text] [PDF]