Novel Regulation of Vascular Endothelial Growth Factor-A (VEGF-A) by Transforming Growth Factor β1

Clifford, Rachel L.; Deacon, Karl; Knox, Alan J.

doi:10.1074/jbc.m803342200

Cited by 92 publications

(78 citation statements)

References 44 publications

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“…Furthermore, AP-2 and Sp1 activate the VEGF promoter in response to several cytokines. In addition to binding sites for Sp1, AP-2, and HIFs, VEGF promoter contains binding sites for the transcription factors NF-κB, NF-1, TCF, Egr-1, and AP-1 (21). In the present study, immunoblotting revealed that S1P enhances the expression of c-Jun and c-Fos and activates c-Jun.…”

Section: Ap-1 Is Important For S1p-mediated Vegf Inductionmentioning

confidence: 56%

Sphingosine 1-phosphate induces vesicular endothelial growth factor expression in endothelial cells

Heo¹,

Park²,

Kim³

et al. 2009

BMB Reports

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Angiogenesis is essential for tumor growth and vascular endothelial cell growth factor (VEGF) plays a key role in this process. Conversely, sphingosine 1-phosphate (S1P) is a biologically active sphingolipid known to play a key role in cancer progression by regulating endothelial cell proliferation and migration. In this study, the authors found that S1P increases the level of VEGF mRNA in human umbilical vein endothelial cells (HUVECs) and immortalized HUVECs (iHUVECs). Additionally, S1P was found to increase VEGF promoter activity in MS-1 mouse pancreatic islet endothelial cells. Furthermore, a pharmacological inhibitory study revealed that Gαi/o-mediated phospholipase C, Akt, Erk, and p38 MAPK signaling are involved in this S1P-induced expression of VEGF. A component of AP1 transcription factor is important for S1P-induced VEGF expression. Taken together, these findings suggest that S1P enhances endothelial cell proliferation and migration by upregulating the expression of VEGF mRNA. [BMB reports 2009; 42(10): 685-690]

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Section: Ap-1 Is Important For S1p-mediated Vegf Inductionmentioning

confidence: 56%

Sphingosine 1-phosphate induces vesicular endothelial growth factor expression in endothelial cells

Heo¹,

Park²,

Kim³

et al. 2009

BMB Reports

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“…Currently, there are five families in the mammalian VEGFs including VEGF A-D and placental growth factor (76). VEGF plays a central role in embryogenic vasculogenesis and angiogenesis and is essential for wound healing and endometrium regeneration in adults (76).…”

Section: Vegfmentioning

confidence: 99%

Molecular Mechanisms of Pulmonary Arterial Remodeling

Crosswhite

Sun

2014

Mol Med

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Pulmonary arterial hypertension (PAH) is characterized by a persistent elevation of pulmonary arterial pressure and pulmonary arterial remodeling with unknown etiology. Current therapeutics available for PAH are primarily directed at reducing the pulmonary blood pressure through their effects on the endothelium. It is well accepted that pulmonary arterial remodeling is primarily due to excessive pulmonary arterial smooth muscle cell (PASMC) proliferation that leads to narrowing or occlusion of the pulmonary vessels. Future effective therapeutics will be successful in reversing the vascular remodeling in the pulmonary arteries and arterioles. The purpose of this review is to provide updated information on molecular mechanisms involved in pulmonary arterial remodeling with a focus on growth factors, transcription factors, and epigenetic pathways in PASMC proliferation. In addition, this review will highlight novel therapeutic strategies for potentially reversing PASMC proliferation.

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“…A large number of transcription factors, such as Stat3, AP-1, TCF4, and Smad2/4, participate in the transcriptional regulation of VEGF (Clifford et al 2008). Additionally, the expression of VEGF is affected by a variety of microenvironmental factors, such as hypoxia, acidosis, and oxidative stress, as well as growth factors and cytokines (Samani et al 2007;Sullivan and Graham 2007).…”

Section: Introductionmentioning

confidence: 99%

The synergistic regulation of VEGF-mediated angiogenesis through miR-190 and target genes

Yang

Yin

et al. 2014

RNA

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VEGF is a major contributor to angiogenesis, a vital process in normal growth and development and tumor transition. However, the current clinical efficacy of VEGF inhibitors is limited, and the molecular mechanism underlying VEGF regulation remains to be elucidated. Here we show that miR-190 directly targets a group of angiogenic effectors besides VEGF per se. Noted, these effectors can transcriptionally regulate VEGF expression in an intracellular or intercellular manner, thus demonstrating that miR-190 modulates the VEGF-mediated tumor angiogenesis at three levels. The synergistic effect of miR-190 and its target genes demonstrates a complex but apparently more stable system, allowing for the tight control of the level of VEGF. Finally, we showed that miR-190 significantly suppresses tumor metastasis, especially angiogenesis. Together, these results indicate that miR-190 is a promising antitumor target in clinical applications.

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Novel Regulation of Vascular Endothelial Growth Factor-A (VEGF-A) by Transforming Growth Factor β1

Cited by 92 publications

References 44 publications

Sphingosine 1-phosphate induces vesicular endothelial growth factor expression in endothelial cells

Sphingosine 1-phosphate induces vesicular endothelial growth factor expression in endothelial cells

Molecular Mechanisms of Pulmonary Arterial Remodeling

The synergistic regulation of VEGF-mediated angiogenesis through miR-190 and target genes

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