Influence of Erythropoietin on Microvesicles Derived from Mesenchymal Ste cells(MSC) protecting renal function of Chronic Kidney Disease
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE68665 | GEO | 2015/05/09
SECONDARY ACCESSION(S): PRJNA283410
REPOSITORIES: GEO
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Project description:miRNA profiles of the MSC-MVs and EPO-MVs were analyzed with a quantitative PCR (qPCR)-based array of the whole mice genome. Further analysis revealed differences in the miRNAs of 212 EPO-MVs (fold change ≥ 1.5 compared to the MSC-MVs), which constituted approximately 22.64% of all of the evaluated mouse miRNAs. Of all of the differences, 70.28% of the changes in the EPO-MV group involved upregulation To study the differential miRNA expression in MV and EPO-MV which might contributed to the better treatment in chronic kidney disease, we performed miRNA expression profiling of the culture supernatant of MSC with or without EPO incubation using the miRCURY LNA Array (v.18.0) (Exiqon, Vedbaek, Denmark).
2015-05-09 | E-GEOD-68665 | biostudies-arrayexpress
Project description:The secretion of exosomes/ microvesicles (MVs) is a recently described mechanism of intercellular communication that is based on the transfer of bioactive molecules. Our hypothesis was that mesenchymal stromal cells (MSC) from myelodisplastic syndromes (MDS) patients could modify CD34+ hematopoietic progenitor cells (HPC) properties throughout MVs. The latter were isolated from MSC from MDS patients and healthy donors (HD). MVs were purified by ExoQuick-TC exosome precipitation solution or ultracentrifugation and identified by transmission electron microscopy (TEM) and flow cytometry (FC). Their Micro-RNA content was evaluated by microarrays. Incorporation of MVs into CD34+ cells was analyzed by FC and confocal microscopy (CM). Our results showed that MVs displayed the same immunophenotypic pattern and similar morphology. The content of miRNAS in the MVs from MDS and HD was significantly different. Next, MVs incorporation into HPC was observed, being highest after 24 hours of incubation. We demonstrated that MVs could modify the HPC behavior since the incubation of HPC with MVs led to gene expression modification evaluated by RT-PCR and increased cell viability by FC. In summary, we show that BM-MSC produce MVs with different cargo in MDS compared to HD. These structures can incorporate into HPC and modify their properties.
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Project description:miRNA profiles of the Young-MSC-MVs and Old-MSC-MVs were analyzed with a quantitative PCR (qPCR)-based array of the whole rat genome. Further analysis revealed the expression of miR-344a, miR-133b-3p, miR-294, miR-423-3p, and miR-872-3p was significantly downregulated in Old-MSC-MVs than in Young-MSC-MVs (p<0.05).
2015-08-20 | GSE72198 | GEO
Project description:Administration of exogenous mesenchymal stem cells (MSCs) has been shown to improve the recovery from acute kidney injury (AKI). It has been suggested that the beneficial effect of MSCs is related to the paracrine release of factors favouring proliferation of intrinsic epithelial cells survived to injury rather than to their trans-differentiation. However the factors involved remain to be determined. In the present study we demonstrated that microvesicles (MVs) derived from human bone marrow MSCs are able to stimulate in vitro proliferation and apoptosis resistance of tubular epithelial cells (TEC). In addition, MVs were found to accelerate in vivo the morphological and functional recovery of glycerol induced AKI in SCID mice by inducing TEC proliferation. The effect of MVs on the recovery of AKI was comparable to that of human MSC treatment. In vitro we found that the CD44 and beta1-integrin-dependent incorporation of MVs in TEC was required for their biological action. However, despite their internalization, RNase-treated MVs failed to induce in vitro apoptosis resistance and TEC proliferation, and in vivo recovery from AKI, suggesting an RNA-dependent biological effect. Microarray analysis and quantitative RT-PCR of MV-RNA extract indicated that MVs were shuttling a specific subset of cellular mRNA, such as mRNA associated with the mesenchymal differentiative phenotype and with several cell functions involved in the control of transcription, proliferation, apoptosis and cell immune regulation. These results suggest that MVs derived from MSCs may activate a proliferative program in TEC survived to injury in AKI by an horizontal transfer of mRNA.
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Project description:Adipose derived stem cells (ASCs) were preconditioned with endothelial differentiation medium (EDM) for four days and then incubated in endothelial basal medium (EBM) supplemented with 1% microvesicle (MV)-free FBS for two days. The conditioned medium was harvested for MV isolation. The small RNA extracted from the MVs was used for microRNA array. qPCR gene expression profiling; Two equal-amount small RNA samples were from two independent experiments.
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Project description:Microvesicles (MV) are small membrane-bound particles comprised of exosomes and various sized extracellular vesicles. These are released by a number of cell types. Microvesicles have a variety of cellular functions from communication to mediating growth and differentiation. Microvesicles contain proteins and nucleic acids. Previously, we showed that plasma microvesicles contain microRNAs (miRNAs). Based on our previous report, the majority of peripheral blood microvesicles are derived from platelets while mononuclear phagocytes, including macrophages, are the second most abundant population. Here, we characterized macrophage-derived microvesicles and whether they influenced the differentiation of naM-CM-/ve monocytes. We also identified the miRNA content of the macrophage-derived microvesicles. We found that RNA molecules contained in the macrophage-derived microvesicles were transported to target cells, including monocytes, endothelial cells, epithelial cells and fibroblasts. Furthermore, we found that miR-223 was transported to target cells and was functionally active. Based on our observations, we hypothesize that microvesicles bind to and activate target cells. Furthermore, we find that microvesicles induce the differentiation of macrophages. Thus, defining key components of this response may identify novel targets to regulate host defense and inflammation. We used GeneChip microarrays to examine changes in gene expression induced by MV in primary monocyte-derived macrophages (MDM) and in THP1 cells, and compare this to cells treated with GM-CSF and PMA, respectively. All experiments were done in triplicates. Primary monocytes were collected from buffy coats (BC). The freshly isolated monocytes from three donors (Mono1-3) were either treated with GM-CSF or subjected to RNA isolation. Following treatment, MVs were isolated from the GM-CSF-treated macrophage cultures. RNA was isolated from the remaining cells for profiling (GM1-3). The isolated MVs were then used to treat new BC monocytes for 24 h (BC-GMCSF-MV24). A fraction of the new BC monocytes was subjected to RNA extraction for profiling (BC1-3). For THP1 cells, they were treated with either DMSO or PMA to produce MVs. The MVs were collected and the remaining cells lyzed for RNA extraction and profiling (DMSO1-3 and PMA1-3). The collected MVs from the DMSO or PMA-treated THP1 cells were incubated with new THP1 for 24 h and designated DMSO-MV24 or PMA-MV24. We had a total of 24 samples.
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Project description:We evaluated in a rat model of Donor after Circulatory Death (DCD) the effects of pretransplant kidney conditioning with Mesenchymal Stromal Cells (MSC) or MSC derived microvescicles (MV) on ischemic injury. Fisher rats (F) were used as kidney donors, Transgenic Sprague-Dawley rats expressing Enhanced Green Fluorescence Protein (EGFP) as MSC donors. After 20 min of warm ischemia nephrectomy was performed and kidneys were perfused with Belzer solution (BS), BS supplemented with MSC (MSC) or with MV (MV) for 4 h, at 4°C. Renal damage was evaluated by histology, renal gene expression by microarray analysis and RT-PCR. Malondialdehyde, lactate, LDH, glucose and pyruvate were measured in effluent fluid. MSC/MV kidneys showed a significant minor global ischemic damage and up-regulation of three genes encoding proteins that improve cell energy metabolism (Isocitrate dehydrogenase 2, NADH dehydrogenase Fe-S protein 8, Pyruvate dehydrogenase beta) and three genes encoding proteins involved in ion membrane transport (Calbindin 1, Monocarboxylate transporter 1, Vacuolar H+-ATPase d2 subunit). Lactate, LDH and malondialdehyde in effluent fluid were significantly lower in MSC/MV kidneys than BS. Glucose was lower while pyruvate higher in MSC/MV effluent than BS, suggesting a larger use of energy substrates by MSC/MV kidneys. MSC/MV perfusion of kidneys in addition to BS through HMP protects from ischemia injury by preserving the enzymatic machinery essential for cell viability and prepares kidney to reperfusion damage.
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Project description:Circulating microvesicles (MVs) have been described as important players in cell-to-cell communication carrying biological information both in normal and pathologic condition. MVs released by cancer cells may incorporate biomolecules such as active lipids, proteins and RNA, which can be delivered and internalized by recipient cells potentially altering gene expression of receiving cells eventually impacting disease progression. In this study, we took advantage of a leukemia in vitro model to investigate MVs as vehicles of protein coding messages. Leukemic cell lines (K562, REH and SHI-1) carrying recurrent translocations were analyzed. In the leukemic cells these translocations are transcribed into oncogenic fusion transcripts. Here, using gene expression microarrays we monitored leukemic fusion transcripts as hallmarks of leukemic cells transcriptome to track mRNA transfer from parental cells to MVs. Transcriptome analysis of K562 cells and released MVs disclosed MVs as not just “small scale cells”. In fact, a number of transcripts related to membrane activity, cell surface receptors and extracellular communication were enriched in the MVs pool. On the other hand, sets of transcripts related to the basal cellular functions and transcripts of the BCR-ABL oncogenic pathway downstream of the fusion protein were detected in MVs as well as in parental K562 cells. Moreover, through co-culture analyses uptake of leukemic MVs in receiving cells was confirmed and an MV-dosage dependent increase of target cell proliferation was demonstrated. Our study provides novel understanding of tumor-derived MVs as carrier of protein coding messages. For the first time a whole transcriptome gene expression analysis has been performed comparing K562 parental cells and released MVs, showing an enrichment of transcripts coding for oncogenic proteins and for proteins involved in key cellular pathways.
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