Growth factors and angiogenesis

Schott, Robert J.; Morrow, Linda

doi:10.1093/cvr/27.7.1155

Cited by 91 publications

(35 citation statements)

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“…In addition, they have been considered to be part of mechanisms responsible for angiogenic, antiapoptotic, and mitogenic effects after cell transplantation [51,52]. Similar to previous studies, our current study showed that VEGF, which is best known as a key mitogen for ECs [53,54], could promote the proliferation of ECs in vitro. Interestingly, IGF-1, which had a proangiogenic effect [55], increased noticeably in BMMCs-CM, and it was found that IGF-1 was also related to cell proliferation of ECs in vitro.…”

Section: Discussionsupporting

confidence: 88%

Bone Marrow Mononuclear Cells Promote Proliferation of Endogenous Neural Stem Cells Through Vascular Niches After Cerebral Infarction

et al. 2010

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Increasing evidence shows that administration of bone marrow mononuclear cells (BMMCs) is a potential treatment for various ischemic diseases, such as ischemic stroke. Although angiogenesis has been considered primarily responsible for the effect of BMMCs, their direct contribution to endothelial cells (ECs) by being a functional elements of vascular niches for neural stem/progenitor cells (NSPCs) has not been considered. Herein, we examine whether BMMCs affected the properties of ECs and NSPCs, and whether they promoted neurogenesis and functional recovery after stroke. We compared i.v. transplantations 1 3 10 6 BMMCs and phosphate-buffered saline in mice 2 days after cortical infarction. Systemically administered BMMCs preferentially accumulated at the postischemic cortex and periinfarct area in brains; cell proliferation of ECs (angiogenesis) at these regions was significantly increased in BMMCstreated mice compared with controls. We also found that endogenous NSPCs developed in close proximity to ECs in and around the poststroke cortex and that ECs were essential for proliferation of these ischemia-induced NSPCs. Furthermore, BMMCs enhanced proliferation of NSPCs as well as ECs. Proliferation of NSPCs was suppressed by additional treatment with endostatin (known to inhibit proliferation of ECs) following BMMCs transplantation. Subsequently, neurogenesis and functional recovery were also promoted in BMMCs-treated mice compared with controls. These results suggest that BMMCs can contribute to the proliferation of endogenous ischemia-induced NSPCs through vascular niche regulation, which includes regulation of endothelial proliferation. In addition, these results suggest that BMMCs transplantation has potential as a novel therapeutic option in stroke treatment.

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Section: Discussionsupporting

confidence: 88%

Bone Marrow Mononuclear Cells Promote Proliferation of Endogenous Neural Stem Cells Through Vascular Niches After Cerebral Infarction

et al. 2010

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“…Numerous angiogenic factors have been identified (3,61). Which growth factor(s) are responsible for induction of angiogenesis by Nf1-deficient Schwann cells has not been addressed in this study.…”

Section: Discussionmentioning

confidence: 98%

Nf1-Deficient Mouse Schwann Cells Are Angiogenic and Invasive and Can Be Induced To Hyperproliferate: Reversion of Some Phenotypes by an Inhibitor of Farnesyl Protein Transferase

Kim

Ling

Ratner

1997

Molecular and Cellular Biology

136

120

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We have developed a potential model of Schwann cell tumor formation in neurofibromatosis type 1 (NF1). We show that mouse Schwann cells heterozygous or null at Nf1 display angiogenic and invasive properties, mimicking the behavior of Schwann cells from human neurofibromas. Mutations at Nf1 are insufficient to promote Schwann cell hyperplasia. Here we show that Schwann cell hyperplasia can be induced by protein kinase A activation in mutant cells. Removal of serum from the culture medium also stimulates hyperplasia, but only in some mutant cells. After serum removal, clones of hyperproliferating Schwann cells lose contact with axons in vitro, develop growth factor-independent proliferation, and exhibit decreased expression of the cell differentiation marker P0 protein; hyperproliferating cells develop after a 1-week lag in Schwann cells heterozygous at Nf1. The experiments suggest that events subsequent to Nf1 mutations are required for development of Schwann cell hyperplasia. Finally, an anti-Ras farnesyl protein transferase inhibitor greatly diminished both clone formation and hyperproliferation of null mutant cells, but not invasion; farnesyl transferase inhibitors could be useful in treating benign manifestations of NF1.Neurofibromatosis type 1 (NF1) is one of the most common inherited human autosomal dominant diseases, with a worldwide incidence of 1 in 3,500 individuals (56). Benign manifestations frequently associated with NF1 include pigmented lesions of the skin (café au lait spots), hamartomas of the iris (Lisch nodules), learning disabilities, formation of optic pathway gliomas, and neurofibromas (22). Neurofibromas are one of the major defining features of NF1. Cutaneous neurofibromas (benign peripheral nerve sheath tumors) are associated with small nerve branches, plexiform neurofibromas develop along major peripheral nerves, and malignant peripheral nerve sheath tumors (MPNST) develop in about 4% of NF1 patients (56). Genetic studies show that malignant tumors in NF1, including MPNSTs, contain cells with mutations in both the constitutionally inactivated and previously normal somatic allele, consistent with NF1 acting as a tumor suppressor (19,36,64). The mechanism of neurofibroma formation is less clear. While recent studies demonstrated loss of heterozygosity (LOH) at the NF1 locus in some neurofibromas (12, 60), LOH could be associated with either of the major cell types in the benign tumors, fibroblasts or Schwann cells.Schwann cells may be the primary pathogenic cells in neurofibromas. The majority (40 to 85%) of cells in neurofibromas are Schwann cells (18,49), and in contrast to Schwann cells in normal nerve, neurofibroma Schwann cells are found without association with axons (28, 50). Furthermore, in vitro, Schwann cells, but not fibroblasts, from neurofibromas show angiogenic and invasive properties (63). Because the genetic status of neurofibroma Schwann cells is unknown, it remains unclear if a single NF1 mutation is sufficient for manifestation of some neurofibroma Schwann cell phenotype...

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“…VEGF, also known as vascular permeability factor, is expressed in response to hypoxia and other stimuli by a variety of differentiated cells (1, 2, 6 -14). VEGF expression has also been found in numerous human and rodent transformed cells (3,4,(15)(16)(17)(18)(19). VEGF is encoded by a single gene, but it exists in four isoforms of 121, 165, 189, and 206 amino acids due to alternative mRNA splicing (20,21).…”

Section: Vegfmentioning

confidence: 99%

“…In addition to VEGF, PLGF has also been demonstrated to bind FLT-1 with high affinity, but not to KDR/Flk-1 (34,35). VEGF is a potent endothelial cell mitogen in vitro, while PLGF is 3 orders of magnitude less potent at inducing endothelial cell proliferation (4,(15)(16)(17)(18). However, PLGF can significantly potentiate the in vitro and in vivo activity of low concentrations of VEGF (34).…”

mentioning

confidence: 99%

Identification of Vascular Endothelial Growth Factor Determinants for Binding KDR and FLT-1 Receptors

Keyt¹,

Nguyen²,

Berleau³

et al. 1996

Journal of Biological Chemistry

439

314

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Growth factors and angiogenesis

Cited by 91 publications

References 0 publications

Bone Marrow Mononuclear Cells Promote Proliferation of Endogenous Neural Stem Cells Through Vascular Niches After Cerebral Infarction

Bone Marrow Mononuclear Cells Promote Proliferation of Endogenous Neural Stem Cells Through Vascular Niches After Cerebral Infarction

Nf1-Deficient Mouse Schwann Cells Are Angiogenic and Invasive and Can Be Induced To Hyperproliferate: Reversion of Some Phenotypes by an Inhibitor of Farnesyl Protein Transferase

Identification of Vascular Endothelial Growth Factor Determinants for Binding KDR and FLT-1 Receptors

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