Similar Datasets
Project description:Gene expression in p75NTR knockout mouse liver
| PRJNA505171 | ENA
Project description:Proteome comparison between bone-marrow cells isolated from wildtype and NUDT2 knockout mice.
2021-11-03 | PXD023219 | Pride
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
2008-07-17 | GSE9910 | GEO
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
Project description:In situ synthesized oligo arrays, U74Av2, from Affymetrix were used to measure differential gene expression in RNA samples generated from the liver of Nrf2 knockout and wildtype mice at 5 month age. Total RNAs from two Nrf2 knockout or wildtype littermates were analyzed separately. There are two replicates (GSM 13431, 13435) for the female Nrf2 wildtype group, two replicates (GSM 13439, 13441) for the male Nrf2 wildtype group, two replicates (GSM 13436, 13437) for the female Nrf2 knockout group, and two replicates (GSM 13438, 13440) for the male Nrf2 knockout group. Keywords: parallel sample
2003-12-16 | GSE864 | GEO
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
Project description:Transcriptomics analysis of gene expression in wildtype and FTO knockout mouse liver
| PRJNA517498 | ENA
Project description:In the project « VLK in liver protection », we analyzed conditioned medium and whole cell lysate of Y/A/C-treated hepatocytes isolated from wildtype (WT) and VLK knockout (KO) mice, three biological replicates each.
2022-03-24 | PXD031378 | Pride
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.
2014-01-11 | GSE53899 | GEO
Project description:Kynurenine monooxygenase (KMO) knockout mouse liver transcriptomics
| PRJEB62865 | ENA