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Effect of neurotrophin p75 receptor (p75NTR) on angiogenesis

ABSTRACT: Neurotrophins (NTs) promotes angiogenesis and EC survival, via tropomyosin kinase trkA and trkB receptors. A different p75NTR receptor of NTs, which belongs to the TNF-alfa receptor superfamily, is not or scarcely expressed by endothelial cells (EC) and endothelial progenitor cells (EPC) under basal conditions. Both diabetes and muscular ischemia induce p75NTR in capillary EC. In this study, by gene transfer, we forced the expression of p75NTR in EC and EPC to study the effect on cell survival, proliferation, adhesion, migration, and capillary-like tubes formation on matrigel, which all resulted impaired by p75NTR. We identified that p75NTR inhibits the VEGF-A/Akt/eNOS/NO pro-angiogenesis/pro-EC survival pathway and reduces the mRNA contents of survivin and securin in EC. By Illumina technology and real-time PCR, we found that p75-NTR alters the expression of VEGF-A and beta-1 integrin, which are implicated in angiogenesis and cell survival. p75NTR transfer to ischemic murine limb muscles impaired neoangiogenesis and blood flow recovery and induced apoptosis of bone marrow Sca-1+/Lin- progenitor cells. Diabetes induced p75NTR in bone marrow Sca-1+/Lin- cells and this correlated with apoptosis. Finally, inhibition of p75NTR signaling in diabetic ischemic limb muscles restored proper muscular neovascularization and blood flow recovery. Keywords: Response to ectopic receptor expression on angiogenesis

ORGANISM(S): Mus musculus

PROVIDER: GSE9910 | GEO | 2008/07/17

SECONDARY ACCESSION(S): PRJNA103899

REPOSITORIES: GEO

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Effect of neurotrophin p75 receptor (p75NTR) on angiogenesis

Project description:Neurotrophins (NTs) promotes angiogenesis and EC survival, via tropomyosin kinase trkA and trkB receptors. A different p75NTR receptor of NTs, which belongs to the TNF-alfa receptor superfamily, is not or scarcely expressed by endothelial cells (EC) and endothelial progenitor cells (EPC) under basal conditions. Both diabetes and muscular ischemia induce p75NTR in capillary EC. In this study, by gene transfer, we forced the expression of p75NTR in EC and EPC to study the effect on cell survival, proliferation, adhesion, migration, and capillary-like tubes formation on matrigel, which all resulted impaired by p75NTR. We identified that p75NTR inhibits the VEGF-A/Akt/eNOS/NO pro-angiogenesis/pro-EC survival pathway and reduces the mRNA contents of survivin and securin in EC. By Illumina technology and real-time PCR, we found that p75-NTR alters the expression of VEGF-A and beta-1 integrin, which are implicated in angiogenesis and cell survival. p75NTR transfer to ischemic murine limb muscles impaired neoangiogenesis and blood flow recovery and induced apoptosis of bone marrow Sca-1+/Lin- progenitor cells. Diabetes induced p75NTR in bone marrow Sca-1+/Lin- cells and this correlated with apoptosis. Finally, inhibition of p75NTR signaling in diabetic ischemic limb muscles restored proper muscular neovascularization and blood flow recovery. Keywords: Response to ectopic receptor expression on angiogenesis Two series of 4 mice each were treated with either control adenovirus (AdNull) or adenovirus expressing neurotrophin p75 receptor (AdP75). Anaesthetized mice received 3 adenovirus injections (for a total of 109 p.f.u. virus in 20 micro L) into 3 equidistant sites of the normoperfused or ischemic left adductor muscles, as described (2. Emanueli C, Graiani G, Salis MB, Gadau S, Desortes E, Madeddu P. Prophylactic gene therapy with human tissue kallikrein ameliorates limb ischemia recovery in type 1 diabetic mice. Diabetes. 2004 Apr;53(4):1096-103. )

2010-06-25 | E-GEOD-9910 | biostudies-arrayexpress

Effect of neurotrophin receptor p75 (p75NTR) over-expression on the miRNAome of human umbilical vein endothelial cells

Project description:MicroRNAs (miRNAs) are small non-protein-coding RNAs that are incorporated into the RNA-induced silencing complex (RISC) and inhibit gene expression by regulating the stability and/or the translational efficiency of target mRNAs. p75NTR, which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. p75NTR expression promotes endothelial cells apoptosis and inhibits angiogenesis. In order to identify miRNAs sub-sequentely modulated by p75NTR, miRNA expression profiles of human umbilical vein endothelial cells (HUVEC) over-expressing p75NTR were generated, allowing the identification of miRNAs modulated upon p75NTR up-regulation. HUVEC over-expressing p75NTR or Null (empty vector) were generated by adenoviral infection. miRNA expression profiles were then measured and miRNAs modulated upon p75NTR up-regulation were identified.

2014-01-11 | E-GEOD-53899 | biostudies-arrayexpress

Effect of neurotrophin receptor p75 (p75NTR) over-expression on the miRNAome of human umbilical vein endothelial cells

2014-01-11 | GSE53899 | GEO

Identification of targets regulated by SELP in HSC

2014-05-09 | GSE57459 | GEO

Gene expression profiling in WT and Hif1a-/- HSCs

Project description:To understand the underlying mechanism by which the Hif1a gene is required by hematopoietic stem cells (HSCs), we performed a comparative DNA microarray analysis using total RNA isolated from wild type Lin-Sca-1+c-Kit+ cells and Hif1a-/- Lin-Sca-1+c-Kit+ cells. The result was validated by quantitative real-time PCR analysis of wild type Lin-Sca-1+c-Kit+ and Hif1a-/- Lin-Sca-1+c-Kit+ cells.

2012-04-04 | GSE35110 | GEO

RNA-seq analysis of mouse pluripotent stem cells derived cells

Project description:To detect the role of OP9 stromal cells in our optimized 3D self-assembling peptide induction system followed by the OP9 coculture system. First, we used RNA-seq to analyze mouse pluripotent stem cells derived total cells at day5 between the 3D+OP9 and 3D+0.1% group in our hematopoietic differentiation system. In addition, to further evaluate hematopoietic transcriptome differences between Lin-Sca-1+c-kit+CD201+ cells and Lin-Sca-1+c-kit+CD201- cells, we used RNA-seq to analyze mouse pluripotent stem cells derived Lin-Sca-1+c-kit+CD201+ and Lin-Sca-1+c-kit+CD201- cells at day5 in our 3D+OP9 hematopoietic differentiation system.Meanwhile,we used the mouse embryonic stem cell(mESC) as negative control and bone marrow derived Lin-Sca-1+c-kit+CD201+ and fetal liver derived Lin-Sca-1+c-kit+CD201+ as positive control.

2021-06-28 | GSE175563 | GEO

Identification of targets regulated by SELP in HSC

2014-05-09 | E-GEOD-57459 | biostudies-arrayexpress

Gene expression data of Lsd1fl/fl and Lsd1fl/fl Mx1Cre CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs

Project description:We discovered that mice that lack Lsd1 in hematopoietic cells were exhibited increased frequencies of CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs, but completely lacked the lin- c-Kit+ Sca-1- myeloid progenitor compartment. To determine the genes altered by Lsd1-loss, CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs from Lsd1fl/fl and Lsd1fl/fl Mx1Cre mice were FACS-purified to be analyzed by gene expression profiling.

2013-06-25 | GSE40284 | GEO

Gene expression profiling of mouse prostate stem cells

Project description:The mouse prostate tissue exhibits strong power of regeneration, indicating the exisistence of prostate stem cells. Previously we showed that a single mouse prostate cells defined by Lin-CD44+CD133+Sca-1+CD117+ phenotype can generate a prostate after transplantation in vivo. In this study, we compared gene expression profiles of mouse prostate stem cells ( Lin-CD44+CD133+Sca-1+CD117+) and prostate non-stem cells (Lin-CD44-CD133-Sca-1-CD117-).

2011-12-06 | GSE33317 | GEO

Gene expression profiling in WT and Alox15-/- HSCs

Project description:To understand the underlying mechanism by which Alox15 gene is required by HSCs, we performed a comparative DNA microarray analysis using total RNA isolated from wild type Lin-Sca-1+c-Kit+, Alox5-/- Lin-Sca-1+c-Kit+. The result was validated by quantitative real-time PCR analysis of wild type Lin-Sca-1+c-Kit+ and Alox15-/- Lin-Sca-1+c-Kit+. Cancer stem cells are responsible for the initiation and maintenance of some types of cancer, and few effective target genes in these stem cells have been identified. Here we show that the arachidonate 15-lipoxygenase gene (Alox15) is essential for the survival of leukemia stem cells (LSCs) in BCR-ABL-induced chronic myeloid leukemia (CML). In the absence of Alox15, BCR-ABL failed to induce CML in mice. This Alox15 deficiency caused the impairment of LSC function through affecting cell division and apoptosis, leading to eventual deletion of LSCs. Inhibition of Alox15 function by a chemical compound also impaired the function of LSCs, and cured CML mice. In addition, we show that Alox15 is required for the survival of human CD34+ CML stem cells. The defective CML phenotype in the absence of Alox15 is rescued by depleting P-selectin. The underlying mechanisms are also related to pathways involving PTEN, PI3K/AKT, and ICSBP. These results identify Alox15 as a potential target gene for eradicating LSCs in CML, providing a novel strategy for treating CML patients for cure.

2011-05-17 | GSE29348 | GEO

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