VEGF-C is a trophic factor for neural progenitors in the vertebrate embryonic brain

Bras, Barbara Le; Barallobre, Marı́a José; Homman‐Ludiye, Jihane; Ny, Annelii; Wyns, Sabine; Tammela, Tuomas; Haiko, Paula; Karkkainen, Marika J.; Li, Yuan; Muriel, Marie‐Paule; Chatzopoulou, Elli; Bréant, Christiane; Zalc, Bernard; Carmeliet, Peter; Alitalo, Kari; Eichmann, Anne; Thomas, Jean‐Léon

doi:10.1038/nn1646

Cited by 165 publications

(128 citation statements)

References 47 publications

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“…Targeted mutagenesis of the VEGF-A promoter region results in motoneuron death and the development of amyotrophic lateral sclerosis-like disease (Oosthuyse et al 2001). Recently, VEGF-C signaling through VEGFR-3 was shown to play a role in oligodendrocyte development (Le Bras et al 2006). Thus, an ancient role of a common PDGF/VEGF ancestor in neural development may have evolved into roles for both PDGFs and VEGFs in oligodendrocyte development and neuroprotection.…”

Section: Role Of Pdgfs In Glial Cell Development and Neuroprotectionmentioning

confidence: 99%

Role of platelet-derived growth factors in physiology and medicine

Andræ¹,

Gallini²,

Betsholtz³

2008

Genes Dev.

2,031

1,898

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Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) have served as prototypes for growth factor and receptor tyrosine kinase function for more than 25 years. Studies of PDGFs and PDGFRs in animal development have revealed roles for PDGFR-␣ signaling in gastrulation and in the development of the cranial and cardiac neural crest, gonads, lung, intestine, skin, CNS, and skeleton. Similarly, roles for PDGFR-␤ signaling have been established in blood vessel formation and early hematopoiesis. PDGF signaling is implicated in a range of diseases. Autocrine activation of PDGF signaling pathways is involved in certain gliomas, sarcomas, and leukemias. Paracrine PDGF signaling is commonly observed in epithelial cancers, where it triggers stromal recruitment and may be involved in epithelial-mesenchymal transition, thereby affecting tumor growth, angiogenesis, invasion, and metastasis. PDGFs drive pathological mesenchymal responses in vascular disorders such as atherosclerosis, restenosis, pulmonary hypertension, and retinal diseases, as well as in fibrotic diseases, including pulmonary fibrosis, liver cirrhosis, scleroderma, glomerulosclerosis, and cardiac fibrosis. We review basic aspects of the PDGF ligands and receptors, their developmental and pathological functions, principles of their pharmacological inhibition, and results using PDGF pathway-inhibitory or stimulatory drugs in preclinical and clinical contexts.Platelet-derived growth factor (PDGF) was identified more than three decades ago as a serum growth factor for fibroblasts, smooth muscle cells (SMCs), and glia cells (Kohler and Lipton 1974;Ross et al. 1974;Westermark and Wasteson 1976). Human PDGF was originally identified as a disulfide-linked dimer of two different polypeptide chains, A and B, separable using reversed phase chromatography (Johnsson et al. 1982). The B-chain (PDGF-B) was characterized by amino acid sequencing, revealing a close homology between PDGF-B and the product of the retroviral oncogene v-sis of simian sarcoma virus (SSV) (Doolittle et al. 1983;Waterfield et al. 1983). Subsequent studies confirmed that the human cellular counterpart (c-sis) was identical to PDGF-B and that autocrine PDGF activity was sufficient for SSV transformation in vitro. This was a paradigm-shifting discovery about the relationship between neoplastic cell transformation and normal growth control. For the first time, the importance of autocrine growth stimulation in neoplastic transformation was demonstrated. As discussed below, it is now well established that autocrine PDGF stimulation plays a role also in some human cancers.PDGF-A was characterized by cDNA cloning ). This resolved a paradoxical lack of correlation between secretion of PDGF-like growth factors from tumor cell lines and their expression of c-sis; it turned out that most such cell lines express PDGF-A and secrete PDGF-AA homodimers ). Together with the demonstration that PDGF-BB homodimers are produced by SSV-transformed or PDGF-Bexpressing cells, these results showed that the PDGF...

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Section: Role Of Pdgfs In Glial Cell Development and Neuroprotectionmentioning

confidence: 99%

Role of platelet-derived growth factors in physiology and medicine

Andræ¹,

Gallini²,

Betsholtz³

2008

Genes Dev.

2,031

1,898

View full text Add to dashboard Cite

show abstract

“…Although VEGF is best known for its role as a growth factor for endothelial cells, its receptors are also expressed by neurons (13). VEGF prolongs the lifespan of mesencephalic neurons in culture (43) and rescues hippocampal and cortical neurons from serum deprivation (44), hypoxia (45), and glutamate-induced cell death (46). The mechanism by which TNFRI can regulate the expression of VEGF in pMCAO lesions and GD-treated neurons is not yet known.…”

Section: Fig 3 Tnf-and Gd-mediated Induction Of Epor In Neurons Is mentioning

confidence: 99%

TNF receptor I sensitizes neurons to erythropoietin- and VEGF-mediated neuroprotection after ischemic and excitotoxic injury

Taoufik

Petit

Divoux

et al. 2008

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

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CNS neurons use robust cytoprotective mechanisms to ensure survival and functioning under conditions of injury. These involve pathways induced by endogenous neuroprotective cytokines such as erythropoietin (EPO). Recently, in contrast to its well known deleterious roles, TNF has also been shown to exhibit neuroprotective properties. In the present study, we investigated the molecular mechanisms by which TNF receptor (TNFR)I mediates neuroprotection by comparing the gene expression profiles of lesioned cortex from WT and TNFRI KO mice after permanent middle cerebral artery occlusion. Several known neuroprotective molecules were identified as TNFRI targets, notably members of the Bcl-2 family, DNA repair machinery and cell cycle, developmental, and differentiation factors, neurotransmitters and growth factors, as well as their receptors, including EPO receptor (EPOR), VEGF, colony-stimulating factor receptor 1, insulin-like growth factor (IGF), and nerve growth factor (NGF). Further analysis showed that induction of EPOR and VEGF expression in primary cortical neurons after glucose deprivation (GD) largely depended on TNFRI and was further up-regulated by TNF. Also, EPO-and VEGFinduced neuroprotection against GD, oxygen-glucose deprivation, and NMDA excitotoxicity depended significantly on TNFRI presence. Finally, EPO prevented neuronal damage induced by kainic acid in WT but not TNFRI KO mice. Our results identify cross-talk between tissue protective cytokines, specifically that TNFRI is necessary for constitutive and GD-induced expression of EPOR and VEGF and for EPOmediated neuroprotection.cDNA microarray ͉ cytokine signaling ͉ neuron death ͉ transgenic mice ͉ epilepsy

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“…In the SGZ of the adult CNS, mitotic cells are closely associated with blood vessels (Palmer et al, 2000). Endothelial cells in coculture with neural stem cells were found to release soluble factors that increase self-renewal of the stem cells, an effect that is likely to be mediated through VEGF-C/VEGFR-3 and/or pigment epithelium derived factor (PEDF) (Shen et al, 2004;Le Bras et al, 2006;Ramirez-Castillejo et al, 2006) Additionally, basal-lamina-like extensions (called fractones) extend from blood vessels in the SEZ and make contact with all cells in the niche providing a source of ECM containing collagen-IV, laminins, perlecan, nidogen and, in some cases, heparan sulfate proteoglycans (HSPG). These likely send important signals to the stem cells that may include the presentation of FGF-2, which binds to fractone HSPG (Mercier et al, 2002;Kerever et al, 2007).…”

Section: Signaling In Adult Neural and Other Stem Cell Nichesmentioning

confidence: 99%

The microenvironment of the embryonic neural stem cell: Lessons from adult niches?

Lathia

Rao

Mattson

et al. 2007

Developmental Dynamics

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A better understanding of the signals regulating embryonic neural stem cells is clearly an important goal. However, many studies on neural stem cell biology are conducted on the slowly-dividing cells found in the adult CNS, where specialized microenvironments or niches maintain the stem cells throughout life. By contrast, the embryonic VZ is a transient structure that does not fulfill the criteria conventionally used to define niches. In this review we will examine whether, despite these differences, the signals found in other adult stem cell niches are present in the VZ. Using the similarities and differences we observe, we will reconsider whether the location of embryonic stem cell populations such as the VZ can be thought of as niches. Finally, we will ask how these lessons from the niche inform our understanding of neurodevelopmental diseases and cancers of the CNS. Developmental Dynamics 236:3267-3282, 2007.

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VEGF-C is a trophic factor for neural progenitors in the vertebrate embryonic brain

Cited by 165 publications

References 47 publications

Role of platelet-derived growth factors in physiology and medicine

Role of platelet-derived growth factors in physiology and medicine

TNF receptor I sensitizes neurons to erythropoietin- and VEGF-mediated neuroprotection after ischemic and excitotoxic injury

The microenvironment of the embryonic neural stem cell: Lessons from adult niches?

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