Placenta growth factor stimulates MAP kinase and mitogenicity but not phospholipase C-γ and migration of endothelial cells expressing Flt 1

Landgren, Eva; Schiller, Petter; Cao, Yihai; Claesson‐Welsh, Lena

doi:10.1038/sj.onc.1201545

Cited by 153 publications

(114 citation statements)

References 24 publications

Supporting

Mentioning

108

Contrasting

Unclassified

Order By: Relevance

“…Activation of the p42/44 MAP kinase pathway by VEGF and subsequent cell proliferation has been documented for many types of endothelial cells (Seetharam et al, 1995;D'Angelo et al, 1995;Rousseau et al, 1997;Kroll and Waltenberger, 1997;Takahashi and Shibuya, 1997;Landgren et al, 1998;Takahashi et al, 1999). Association of VEGFR-2 with Grb2 suggests that activated Ras might be involved in the regulation of the VEGF-induced mitogenic response.…”

Section: Vegfr-2mentioning

confidence: 99%

“…Nevertheless, there is still a considerable controversy regarding the role of VEGFR-1 in endothelial cells. For example, it has been reported that in VEGFR-1-transfected endothelial cells PlGF but not VEGF could activate the MAPK pathway to induce a mitogenic response and plasminogen activator production (Landgren et al, 1998). Another report suggests that VEGFR-1 might be important for endothelial cell migration.…”

Section: Vegfr-1mentioning

confidence: 99%

See 1 more Smart Citation

Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis

2000

View full text Add to dashboard Cite

Section: Vegfr-2mentioning

confidence: 99%

Section: Vegfr-1mentioning

confidence: 99%

Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis

2000

View full text Add to dashboard Cite

“…Data are mean ± SD. Statistical analysis was the unpaired Student t test comparing each VEGF Δ or VEGF f/f DOX treatment day to comparably treated NTG controls: *P < 0.05, **P < 0.01 and ***P < 0.001. proteins distinct from VEGFR2 in endothelial cells (42,43). PlGF has been shown to amplify or inhibit VEGF signaling through multiple mechanisms (44,45).…”

Section: Discussionmentioning

confidence: 99%

VEGF is essential for hypoxia-inducible factor-mediated neovascularization but dispensable for endothelial sprouting

Oladipupo¹,

Kovalski³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

159

117

View full text Add to dashboard Cite

Although our understanding of the molecular regulation of adult neovascularization has advanced tremendously, vascular-targeted therapies for tissue ischemia remain suboptimal. The master regulatory transcription factors of the hypoxia-inducible factor (HIF) family are attractive therapeutic targets because they coordinately up-regulate multiple genes controlling neovascularization. Here, we used an inducible model of epithelial HIF-1 activation, the TetON-HIF-1 mouse, to test the requirement for VEGF in HIF-1 mediated neovascularization. TetON-HIF-1, K14-Cre, and VEGF flox/flox alleles were combined to create TetON-HIF-1:VEGF Δ mice to activate HIF-1 and its target genes in adult basal keratinocytes in the absence of concomitant VEGF. HIF-1 induction failed to produce neovascularization in TetON-HIF-1:VEGF Δ mice despite robust up-regulation of multiple proangiogenic HIF targets, including PlGF, adrenomedullin, angiogenin, and PAI-1. In contrast, endothelial sprouting was preserved, enhanced, and more persistent, consistent with marked reduction in Dll4-Notch-1 signaling. Optical-resolution photoacoustic microscopy, which provides noninvasive, label-free, high resolution, and wide-field vascular imaging, revealed the absence of both capillary expansion and arteriovenous remodeling in serially imaged individual TetON-HIF-1:VEGF Δ mice. Impaired TetON-HIF-1:VEGF Δ neovascularization could be partially rescued by 12- O -tetradecanoylphorbol-13-acetate skin treatment. These data suggest that therapeutic angiogenesis for ischemic cardiovascular disease may require treatment with both HIF-1 and VEGF.

show abstract

“…This is the case for macrophages, which predominantly/exclusively express FLT1 (Clauss et al 1996;Sawano et al 2001), but also for endothelial cells (Landgren et al 1998;Autiero et al 2003), which up-regulate FLT1 in pathological conditions (Shibuya 2006;Huang et al 2007;Vanheule et al 2010;FryszNaglak et al 2011). As shown by mass spectrometry, PlGF and VEGF induce phosphorylation of distinct tyrosine residues of FLT1 (Autiero et al 2003), further underlining that PlGF and VEGF transmit distinct angiogenic signals through FLT1.…”

Section: Molecular Mechanismsmentioning

confidence: 99%

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

Dewerchin¹,

Carmeliet²

2012

Cold Spring Harbor Perspectives in Medicine

196

176

View full text Add to dashboard Cite

Placenta growth factor stimulates MAP kinase and mitogenicity but not phospholipase C-γ and migration of endothelial cells expressing Flt 1

Cited by 153 publications

References 24 publications

Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis

Vascular endothelial growth factor receptors in the regulation of angiogenesis and lymphangiogenesis

VEGF is essential for hypoxia-inducible factor-mediated neovascularization but dispensable for endothelial sprouting

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

Contact Info

Product

Resources

About