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Effects of brain-derived neurotrophic factor on microRNA expression profile in human endothelial progenitor cells

ABSTRACT: Effects of brain-derived neurotrophic factor on microRNA expression profile in human endothelial progenitor cells

PROVIDER: PRJNA420991 | ENA |

REPOSITORIES: ENA

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Effects of brain-derived neurotrophic factor on microRNA expression profile in human endothelial progenitor cells

Project description:The mechanisms underlying proangiogenic function of brain-derived neurotrophic factor (BDNF) are not fully understood. Current study was designed to explore the miRNA profile in human early endothelial progenitor cells (EPCs, also referred to as CFU-Hill cells) in response to BDNF treatment.

2017-12-05 | GSE107667 | GEO

Effects of Brain-Derived Neurotrophic Factor on MicroRNA Expression Profile in Human Endothelial Progenitor Cells.

Project description: Not available

| S-EPMC6050915 | biostudies-literature

microRNA expression in microvesicles (MVs) derived from endothelial progenitor cells (EPCs)

Project description:Evaluation of microRNA expression profile of microvesicles (MVs) derived from endothelial progenitor cells (EPCs) cultured in different oxygen concentrations (normoxic/hypoxic conditions)

2010-12-30 | E-MEXP-2956 | biostudies-arrayexpress

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Project description:microRNA expression profile in endothelial progenitor cells cultured in normoxic and hypoxic condition

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Chemoradiation and Endothelial Progenitor Cells in Colorectal Cancer

Project description:Colorectal cancer (CRC) is one of the common malignancies worldwide, accounting for a significant percentage of cancer mortality. Concurrent chemoradiation (CCRT) is now a standard treatment for unresectable malignancies of anorectum. To improve quality of life, CCRT is also commonly applied in treatment of lower rectal and anal canal cancer to preserve anal sphincter function. The most commonly used chemotherapeutic drugs combined with radiation as radiosensitizers is 5-fluorouracil (5-FU). Circulating endothelial progenitor cells (EPC), which contribute to the tumor vessel formation, reflect the response to chemotherapy both in animal model and clinical trial. Thus, circulating EPC can be used as a marker for optimizing and monitoring the anti-angiogenesis therapy including angiogenesis inhibitors and chemotherapy. Whether circulating EPC can be served as a marker of CCRT efficacy or not remains undetermined. Since CCRT is now a standard treatment of locally advanced and high-risk CRC, the development of a surrogate marker for monitoring CCRT response and optimize treatment intensity is very important. In this grant we intent to monitor the levels of circulating EPC in locally advanced and high-risk CRC patients before, during and after CCRT. To further characterize the changes in function and biology of EPC caused by CCRT, a syngeneic animal model will be also used to evaluate the clonogenecity and specific gene expression of EPC in tumor-bearing mice receiving CCRT.

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RNA sequencing profile of cord blood endothelial progenitor cells

Project description:RNA sequencing profile of cord blood endothelial progenitor cells

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MicroRNA expression profile of human umbilical vein endothelial cells treated with Angiogenin (ANG)

Project description:We quantified differential microRNA (miRNA) expression in Human umbilical vein endothelial cells （HUVECs）response to Angiogenin (ANG) treatment.These data were used to determine which miRNAs are altered on ANG in Human umbilical vein endothelial cells.

2016-12-13 | GSE92256 | GEO

Adenosine-treated endothelial progenitor cells

Project description:The goal of this study was to investigate the effects of the cardioprotective nucleoside adenosine on gene expression in early and late endothelial progenitor cells. Adenosine mod Early outgrowth endothelial progenitor cells were obtained by adhesion of peripheral blood mononuclear cells of healthy volunteers. Late endothelial progenitor cells were obtained by purification of CD34+ peripheral blood cells and were cultured and amplified in endothelial-specific medium containing growth factors. Both cell types were treated by adenosine (10micromol/L) for 6 hours. Total RNA was extracted using conventional Trizol extraction, quantified by Nanodrop and analyzed by Bioanalyzer. 1microg of RNA was amplified using AminoAllyl MessageAmp kit. 5µg amino allyl-coupled RNA was labeled with Cy3 or Cy5 dyes. Dye coupling yield >5% was a prerequisite for further analysis. 750ng of labeled RNA was hybridized on 25,000 gene microarrays for 17 hours at 60°C. 4 arrays per sample were hybridized and scanned with the Genepix 4000B Scanner (Molecular Devices). Six independent experiments were performed. Microarray data quantification and pre-processing was performed with the MAIA software and intensity values were log-transformed. Gene expression values were standardized across experiments with mean = 0 and standard deviation = 1. The SAM tool was applied to identify differentially expressed genes.

2011-01-29 | E-GEOD-26744 | biostudies-arrayexpress

microRNA profile of control vehicle- and coagulation protease factor VIIa-released endothelial extracellular vesicles

Project description:Coagulation protease factor VIIa (FVIIa) is shown to induce anti-inflammatory and barrier protective effects via endothelial cell protein C receptor (EPCR)-dependent, protease-activated receptor-1 (PAR1)-mediated cell signaling. FVII-EPCR-PAR1 signaling also induces the release of extracellular vesicles from endothelial cells. To obtain clues on whether microRNA (miR) carried out by FVIIa-released EEVs contribute to anti-inflammatory and barrier protective effects, we analyzed miR expression in control- and FVIIa-released EEVs by deep sequencing. These data revealed that several anti-inflammatory miR expression was higher (more than 2-fold) in FVIIa-released EEVs compared to control EEVs, the most predominant being miR10a-5p. The differential expression of miR10a-5p and several other abundant miRs were validated by qRT-PCR. Subsequent in vitro and in vivo experiments showed that miR10a in FVIIa-released EEVs contribute to anti-inflammatory and barrier protective effects.

2021-08-29 | GSE182925 | GEO

Brain-derived neurotrophic factor contributes to the cardiogenic potential of adult resident progenitor cells in failing murine heart

Project description:Aims: Resident cardiac progenitor cells show homing properties when injected into the injured but not into the healthy myocardium. The molecular background behind this difference in behavior needs to be studied to elucidate how adult progenitor cells can restore cardiac function of the damaged myocardium. Since the brain-derived neurotrophic factor (BDNF) moderates cardioprotection in injured hearts, we focused on delineating its regulatory role in the damaged myocardium. Methods and Results: Comparative gene expression profiling of freshly isolated undifferentiated Sca-1 progenitor cells derived either from heart failure transgenic αMHC-CyclinT1/Gαq overexpressing mice or wildtype littermates revealed transcriptional variations. Bdnf expression was up-regulated 5-fold during heart failure, which was verified by qRT-PCR and confirmed at the protein level. The migratory capacity of Sca-1 cells from transgenic heart was improved by 15% in the presence of 25ng/ml BDNF. Furthermore, BDNF-mediated effects on Sca-1 cells were studied via pulsed Stable Isotope Labeling of Amino acids in Cell Culture (pSILAC) proteomics approach. After BDNF treatment, significant differences between newly synthesized proteins in Sca-1 cells isolated from control and transgenic mice were observed for CDK1, SRRT, HDGF, and MAP2K3, which are known to regulate cell cycle, survival and differentiation. Moreover, BDNF repressed the proliferation of Sca-1 cells from transgenic hearts. Conclusion: Comparative profiling of resident Sca-1 cells revealed elevated BDNF levels in the failing heart. Exogenous BDNF (i) stimulated migration, which might improve the homing ability of Sca-1 cells derived from the failing heart and (ii) repressed the cell cycle progression suggesting its potency to ameliorate heart failure.

2015-03-26 | GSE58577 | GEO

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