Vascular Endothelial Growth Factor Induces Heparin-binding Epidermal Growth Factor-like Growth Factor in Vascular Endothelial Cells

Arkonac, Burak M.; Foster, Lauren C.; Sibinga, Nicholas E.S.; Patterson, Cam; Lai, Kaihua; Tsai, Jason; Lee, Mu En; Perrella, Mark A.; Haber, Edgar

doi:10.1074/jbc.273.8.4400

Cited by 72 publications

(42 citation statements)

References 49 publications

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“…Cortical precursors of the VZ/SVZ themselves express BDNF, NT-3 (Maisonpierre et al, 1990;Fukumitsu et al, 1998), FGF2 (Raballo et al, 2000), and HB-EGF (Nakagawa et al, 1998). Intriguingly, endothelial cells also express BDNF (Kim et al, 2004), FGF2 (Albuquerque et al, 1998), PDGF, and HB-EGF (Arkonac et al, 1998), and embryonic endothelial cells have recently been shown to promote self-renewal and neurogen-4 (Figure legend continued.) to those shown in a for the percentage of GFP-positive cells present within the cortical plate region. Transfected cells within the SVZ of two littermate pairs, three to four sections per embryo, were counted to obtain these numbers.…”

Section: Discussionmentioning

confidence: 99%

CCAAT/Enhancer-Binding Protein Phosphorylation Biases Cortical Precursors to Generate Neurons Rather Than AstrocytesIn Vivo

Paquin

Barnabé-Heider²,

Kageyama³

et al. 2005

J. Neurosci.

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Section: Discussionmentioning

confidence: 99%

CCAAT/Enhancer-Binding Protein Phosphorylation Biases Cortical Precursors to Generate Neurons Rather Than AstrocytesIn Vivo

Paquin

Barnabé-Heider²,

Kageyama³

et al. 2005

J. Neurosci.

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“…Although HB-EGF is known to have no effect on the proliferation of endothelial cells, some studies demonstrated that VEGF induces expression of angiogenic growth factors, including HB-EGF, in vascular endothelial cells and suggested that HB-EGF induction in response to VEGF provides a critical endothelial cellderived signal, perhaps the activation of the MAPK and AKT cascade, for the process of new blood vessel formation and maturation (39). In addition, the reviews have proposed that HB-EGF acts as one of the recruiting signals for mesenchymal cells during the late phase of angiogenesis (49), implying that HB-EGF plays a critical role in angiogenesis as well as tumor development.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies indicated that HB-EGF can be up-regulated in some pathological states that may involve angiogenesis (37,38). Some studies showed that VEGF, a critical factor in the development of new blood vessels, could induce HB-EGF in vascular endothelial cells and speculated that HB-EGF induction by VEGF may act in a paracrine fashion to promote angiogenesis (39). This prompted us to evaluate …”

Section: Hb-egf Overexpression In Bladder Carcinomas Up-regulates Vegmentioning

confidence: 99%

HB-EGF Is a Potent Inducer of Tumor Growth and Angiogenesis

et al. 2004

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Heparin-binding epidermal growth factor-like growth factor (HB-EGF) has been shown to stimulate the growth of a variety of cells in an autocrine or paracrine manner. Although HB-EGF is widely expressed in tumors compared with normal tissue, its contribution to tumorigenicity is unknown. HB-EGF can be produced as a membrane-anchored form (pro-HB-EGF) and later processed to a soluble form (s-HB-EGF), although a significant amount of pro-HB-EGF remains uncleaved on the cell surface. To understand the roles of two forms of HB-EGF in promoting tumor growth, we have studied the effects of HB-EGF expression in the process of tumorigenesis using in vitro and in vivo systems. We demonstrate here that in EJ human bladder cancer cells containing a tetracycline-regulatable s-HB-EGF or pro-HB-EGF expression system, s-HB-EGF expression increased their transformed phenotypes, including growth rate, colony-forming ability, and activation of cyclin D1 promoter, as well as induction of vascular endothelial growth factor in vitro. Moreover, s-HB-EGF or wild-type HB-EGF induced the expression and activities of the metalloproteases, MMP-9 and MMP-3, leading to enhanced cell migration. In vivo studies also demonstrated that tumor cells expressing s-HB-EGF or wild-type HB-EGF significantly enhanced tumorigenic potential in athymic nude mice and exerted an angiogenic effect, increasing the density and size of tumor blood vessels. However, cells expressing solely pro-HB-EGF did not exhibit any significant tumorigenic potential. These findings establish s-HB-EGF as a potent inducer of tumor growth and angiogenesis and suggest that therapeutic intervention aimed at the inhibition of s-HB-EGF functions may be useful in cancer treatment.

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“…The pathway by which the viral VEGF might induce epidermal proliferation is unclear, but the induction of growth factors, such as fibroblast growth factor 2 (FGF-2), keratinocyte growth factor (KGF), or heparin-binding epidermal growth factor (HB-EGF), is possible. For example, VEGF has been shown to induce HB-EGF in vascular endothelial cells, and HB-EGF is a known mitogen of keratinocytes (2).…”

Section: Discussionmentioning

confidence: 99%

Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

Savory¹,

Stacker

Fleming³

et al. 2000

J Virol

128

116

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Infection by the parapoxvirus orf virus causes proliferative skin lesions in which extensive capillary proliferation and dilation are prominent histological features. This infective phenotype may be linked to a unique virus-encoded factor, a distinctive new member of the vascular endothelial growth factor (VEGF) family of molecules. We constructed a recombinant orf virus in which the VEGF-like gene was disrupted and show that inactivation of this gene resulted in the loss of three VEGF activities expressed by the parent virus: mitogenesis of vascular endothelial cells, induction of vascular permeability, and activation of VEGF receptor 2. We used the recombinant orf virus to assess the contribution of the viral VEGF to the vascular response seen during orf virus infection of skin. Our results demonstrate that the viral VEGF, while recognizing a unique profile of the known VEGF receptors (receptor 2 and neuropilin 1), is able to stimulate a striking proliferation of blood vessels in the dermis underlying the site of infection. Furthermore, the data demonstrate that the viral VEGF participates in promoting a distinctive pattern of epidermal proliferation. Loss of a functional viral VEGF resulted in lesions with markedly reduced clinical indications of infection. However, viral replication in the early stages of infection was not impaired, and only at later times did it appear that replication of the recombinant virus might be reduced.

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Vascular Endothelial Growth Factor Induces Heparin-binding Epidermal Growth Factor-like Growth Factor in Vascular Endothelial Cells

Cited by 72 publications

References 49 publications

CCAAT/Enhancer-Binding Protein Phosphorylation Biases Cortical Precursors to Generate Neurons Rather Than AstrocytesIn Vivo

CCAAT/Enhancer-Binding Protein Phosphorylation Biases Cortical Precursors to Generate Neurons Rather Than AstrocytesIn Vivo

HB-EGF Is a Potent Inducer of Tumor Growth and Angiogenesis

Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

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