Role of VEGF in Developmental Angiogenesis and in Tumor Angiogenesis in the Brain

Machein, Márcia Regina; Plate, Karl H.

doi:10.1007/978-1-4419-8871-3_13

Cited by 22 publications

(33 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The vascular endothelial growth factor (VEGF) and its receptor Flk-1 signaling cascade trigger endothelial growth and angiogenesis during developmental growth and in brain tumors (Machein and Plate 2004). Typically, high levels of VEGF are present in brain tumors providing the tumor with a pro-angiogenic and immunosuppressive environment (Machein and Plate 2004).…”

Section: Tgf-beta and Its Role In Angiogenesis And Tumor Progressionmentioning

confidence: 99%

TGF-beta in neural stem cells and in tumors of the central nervous system

Aigner

Bogdahn

2007

Cell Tissue Res

View full text Add to dashboard Cite

Mechanisms that regulate neural stem cell activity in the adult brain are tightly coordinated. They provide new neurons and glia in regions associated with high cellular and functional plasticity, after injury, or during neurodegeneration. Because of the proliferative and plastic potential of neural stem cells, they are currently thought to escape their physiological control mechanisms and transform to cancer stem cells. Signals provided by proteins of the transforming growth factor (TGF)-beta family might represent a system by which neural stem cells are controlled under physiological conditions but released from this control after transformation to cancer stem cells. TGF-beta is a multifunctional cytokine involved in various physiological and patho-physiological processes of the brain. It is induced in the adult brain after injury or hypoxia and during neurodegeneration when it modulates and dampens inflammatory responses. After injury, although TGF-beta is neuroprotective, it may limit the self-repair of the brain by inhibiting neural stem cell proliferation. Similar to its effect on neural stem cells, TGF-beta reveals anti-proliferative control on most cell types; however, paradoxically, many brain tumors escape from TGF-beta control. Moreover, brain tumors develop mechanisms that change the anti-proliferative influence of TGF-beta into oncogenic cues, mainly by orchestrating a multitude of TGF-beta-mediated effects upon matrix, migration and invasion, angiogenesis, and, most importantly, immune escape mechanisms. Thus, TGF-beta is involved in tumor progression. This review focuses on TGF-beta and its role in the regulation and control of neural and of brain-cancer stem cells.

show abstract

Section: Tgf-beta and Its Role In Angiogenesis And Tumor Progressionmentioning

confidence: 99%

TGF-beta in neural stem cells and in tumors of the central nervous system

Aigner

Bogdahn

2007

Cell Tissue Res

View full text Add to dashboard Cite

show abstract

“…VEGF-A is highly expressed in cancers and serves as the predominant regulator of this pathological angiogenic process, in which VEGF-A has been identified to stimulate vascular endothelial cell growth, survival, and proliferation. It has been also shown to facilitate survival of existing vessels (Machein and Plate, 2004). However, the expression and the role of VEGF-A in the infarcted heart is not well understood.…”

Section: Disscussionmentioning

confidence: 99%

Vascular endothelial growth factor (VEGF)-A: Role on cardiac angiogenesis following myocardial infarction

Zhao

Chen

et al. 2010

Microvascular Research

116

View full text Add to dashboard Cite

The current study is to determine the regulatory role of VEGF-A in cardiac angiogenesis following myocardial infarction (MI). Cardiac angiogenic response and temporal/spatial expression of VEGF-A/VEGF receptors (VEGFR) were examined at 1, 2, 6, 12 hours and 1, 2, 3, 4, 7, 14, and 28 days postMI. We found that following MI, newly formed vessels first appeared at the border zone between noninfarcted and infarcted myocardium as early as day 3 and subsequently in the infarcted myocardium. Vascular density in the infarcted myocardium peaked at day 7 and then gradually declined. VEGF-A mRNA started to increase at the border zone at 2 hours postMI, reached peak at 12 hours, declined at day 1, and returned to normal levels at day 2 and thereafter. VEGF-A protein levels at the border zone were only increased during day 1 postMI. VEGF-A within the infarcted myocardium levels, however, were persistently suppressed postMI. VEGFR expression was significantly increased only at the border zone at day 1, but not in the later stages. The expression of VEGF-A/VEGFR remained unchanged in the noninfarcted myocardium. Thus, the early rise of VEGF-A/VEGFR at the border zone suggests that VEGF-A initiates the cardiac angiogenic response postMI, but short-lived VEGF-A/VEGFR activation at the border zone and consistently suppressed VEGF-A within the infarcted myocardium suggests that VEGF-A may not be crucial to the later stages of angiogenesis.

show abstract

“…Recently, some factors classically known for their effects on the vascular system have been found to influence different steps of adult neurogenesis (Carmeliet, 2003;Eichmann et al, 2005;Raab and Plate, 2007;Zacchigna et al, 2008). These include vascular endothelial growth factor-A (VEGF-A), a major activator of angiogenesis in both embryos (Carmeliet et al, 1996;Ferrara et al, 1996) and tumors (Machein and Plate, 2004), which also has been shown to influence NPCs in vitro and in vivo (Jin et al, 2002;Schänzer et al, 2004;Meng et al, 2006). VEGF-A is a member of the VEGF family that includes six different homologous factors: VEGF-A-VEGF-E and placental growth factor (Raab and Plate, 2007).…”

Section: Introductionmentioning

confidence: 99%

VEGFR-1 Regulates Adult Olfactory Bulb Neurogenesis and Migration of Neural Progenitors in the Rostral Migratory Stream In Vivo

Wittko¹,

Schänzer²,

Kuzmichev³

et al. 2009

Journal of Neuroscience

102

View full text Add to dashboard Cite

The generation of new neurons in the olfactory bulb (OB) persists into adulthood and is a multistep process that includes proliferation, fate choice, migration, survival, and differentiation. Neural precursor cells destined to form olfactory interneurons arise in the subventricular zone (SVZ) and migrate along the rostral migratory stream (RMS) to the OB. Recently, some factors classically known from their effects on the vascular system have been found to influence different steps of adult neurogenesis. In the present study, we report a modulatory function for the vascular endothelial growth factor receptor-1 (VEGFR-1) in adult olfactory neurogenesis. We identified expression of VEGFR-1 in GFAP-positive cells within regions involved in neurogenesis of the adult mouse brain. To determine functions for VEGFR-1 in adult neurogenesis, we compared neural progenitor cell proliferation, migration, and differentiation from wild-type and VEGFR-1 signaling-deficient mice (Flt-1TK Ϫ/Ϫ mice). Our data show that VEGFR-1 signaling is involved in the regulation of proliferation of neuronal progenitor cells within the SVZ, migration along the RMS, and in neuronal differentiation and anatomical composition of interneuron subtypes within the OB. RMS migration in Flt-1TK Ϫ/Ϫ mice was altered mainly as a result of increased levels of its ligand VEGF-A, which results in an increased phosphorylation of VEGFR-2 in neuronal progenitor cells within the SVZ and the RMS. This study reveals that proper RMS migration is dependent on endogenous VEGF-A protein.

show abstract

Role of VEGF in Developmental Angiogenesis and in Tumor Angiogenesis in the Brain

Cited by 22 publications

References 39 publications

TGF-beta in neural stem cells and in tumors of the central nervous system

TGF-beta in neural stem cells and in tumors of the central nervous system

Vascular endothelial growth factor (VEGF)-A: Role on cardiac angiogenesis following myocardial infarction

VEGFR-1 Regulates Adult Olfactory Bulb Neurogenesis and Migration of Neural Progenitors in the Rostral Migratory Stream In Vivo

Contact Info

Product

Resources

About