Characterization of a Novel Form of Angiopoietin-2 (Ang-2B) and Expression of VEGF and Angiopoietin-2 during Chicken Testicular Development and Regression

Mezquita, Jovita; Mezquita, Belén; Pau, Montserrat; Mezquita, Cristóbal

doi:10.1006/bbrc.1999.0934

Cited by 24 publications

(21 citation statements)

References 21 publications

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“…Testicular regression is accompanied by high expression of Ang-2 and very low expression of VEGF (5). Our observations are in accordance with the proposed function of Ang-2 inducing angiogenesis in the presence of VEGF and vascular regression in its absence.…”

supporting

confidence: 91%

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Genomic Structure and Alternative Splicing of Chicken Angiopoietin-2

Mezquita

Pau

et al. 2000

Biochemical and Biophysical Research Communications

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supporting

confidence: 91%

“…Using spermatogenesis as a model of angiogenesis and vascular regression, we have observed high expression of VEGF and Ang-2 in developing immature testis, while the expression of both genes is minimal in adult quiescent mature testis (5). Testicular regression is accompanied by high expression of Ang-2 and very low expression of VEGF (5).…”

mentioning

confidence: 91%

Genomic Structure and Alternative Splicing of Chicken Angiopoietin-2

Mezquita

Pau

et al. 2000

Biochemical and Biophysical Research Communications

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“…Probes for chicken-angiopoietin-1, chicken-angiopoietin-2 (17), and their receptor tie-2 (18) were generated after cloning of cDNA in PCR II, using the Topo cloning kit (Invitrogen). PCR amplification of whole embryo cDNA obtained from a 10-day-old embryo was performed, using the following primers: angiopoietin-1: 5Ј-TGGAACATGTATGGAAAAC-3Ј, forward, and 5Ј-CTCCCAG ACACT-3Ј, reverse; tie-2: 5Ј-GAAGAAGATGCAGTGATCTAC-3Ј, forward, and 5Ј-GAAGTTATGTCCACTGTTTGT, reverse; angiopoietin-2: 5Ј-GATTTCTGTTC AGACCAACGAG-3Ј, forward, and 5Ј-CAGGATTATCTTAAGAACGTAGC-3Ј, reverse (17,19); fibroblast growth factor-2 (FGF-2): 5Ј-TTCTTCCTGCGCATC AAC-3Ј, forward, and 5Ј-CGATAGCTCGTCCAG-3Ј, reverse. Electron microscopy.…”

Section: Methodsmentioning

confidence: 99%

Hyperglycemia-Induced Defects in Angiogenesis in the Chicken Chorioallantoic Membrane Model

et al. 2004

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Diabetes is associated with abnormal angiogenesis. Increased angiogenesis contributes to severe forms of diabetic retinopathy, but angiogenesis is decreased in response to myocardial ischemia in diabetic patients. We evaluated the direct effect of hyperglycemia on angiogenesis in the chicken chorioallantoic membrane assay, a model of active neoangiogenesis. Hyperglycemia, lasting up to 7 days, was induced in 7-day-old chick embryos by a single intravitellus glucose injection. Control embryos received either water (volumic control) or mannitol (osmotic control). Hyperglycemia decreased angiogenesis in this model from the 5th day on. The pattern and expression level of the main vascular growth factors' genes were not altered by hyperglycemia, as assessed by in situ hybridization and semiquantitative RT-PCR. As early as 2 days after hyperglycemia was induced, an increased apoptosis of endothelial cells and pericytes was detected by transferase-mediated deoxyuridine triphosphate nick-end labeling assay and electron microscopy. In the meantime, endothelial cell proliferation was decreased, as assessed by incorporation of bromo-deoxyuridine. Hyperglycemia can therefore impair angiogenesis without altering the expression level of vascular growth factors through induction of apoptosis and decreased proliferation of endothelial cells. Diabetes 53:752-761, 2004

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“…The procedures used for electrophoresis, Northern blot analysis, and preparation of DNA probes have been previously described [Mezquita et al, 1999[Mezquita et al, , 2000. Human VEGFR-1 kinase domain primers were used to obtain a probe that hybridized with the full-length VEGFR-1 mRNA [Mezquita et al, 2003].…”

Section: Preparation Of Rna Electrophoresis Northern Hybridizationmentioning

confidence: 99%

A novel intracellular isoform of VEGFR‐1 activates Src and promotes cell invasion in MDA‐MB‐231 breast cancer cells

Mezquita

Pau

et al. 2010

J of Cellular Biochemistry

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Two types of VEGFR-1 receptors have been characterized: a full-length transmembrane receptor and a truncated extracellular soluble isoform (sVEGFR-1). We report here the characterization, in normal and cancer cells, of a new family of intracellular isoforms of VEGFR-1 resulting from alternative initiation of transcription in intronic sequences of the gene. While the classical isoforms of VEGFR-1 were barely detectable in MDA-MB-231 breast cancer cells, one of the intracellular isoforms transcribed from intron 21 (i(21)VEGFR-1) was the main isoform expressed in these cells. The new transcript encodes for a protein that contains only the phosphotransferase domain and the carboxyterminal tail of VEGFR-1. Treatment of MDA-MB-231 cells with siRNA specific for the tyrosine domain of VEGFR-1 suppressed the expression of i(21)VEGFR-1, downregulated phosphorylation of Src at tyrosine 418, and reduced markedly the invasion capacity of these cells in vitro. Accordingly, overexpression of transfected i(21)VEGFR-1 in MDA-MB-231 cells upregulated the active form of Src and increased invasiveness of MDA-MB-231 cells. The expression of i(21)VEGFR-1 in MDA-MB-231 cells was inhibited by retinoic acid. Both, activation of Src and downregulation by retinoic acid, have been reported in other intracellular members of the Fms/Kit/PDGFR family of tyrosine kinases, particularly in the intracellular isoform of c-kit, analogous structurally to i(21)VEGFR-1 and frequently expressed in cancer cells.

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Characterization of a Novel Form of Angiopoietin-2 (Ang-2B) and Expression of VEGF and Angiopoietin-2 during Chicken Testicular Development and Regression

Cited by 24 publications

References 21 publications

Genomic Structure and Alternative Splicing of Chicken Angiopoietin-2

Genomic Structure and Alternative Splicing of Chicken Angiopoietin-2

Hyperglycemia-Induced Defects in Angiogenesis in the Chicken Chorioallantoic Membrane Model

A novel intracellular isoform of VEGFR‐1 activates Src and promotes cell invasion in MDA‐MB‐231 breast cancer cells

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