Analysis of differential genes in osteogenic induction of alveolar bone derived MSCs under TNFα-induced inflammation in Ccrl2-KO mice and WT mice.
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ABSTRACT:
PROVIDER: PRJNA1046081 | ENA |
REPOSITORIES: ENA
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Project description:In order to explore the effect of Ccrl2 knockout on the osteogenic differentiation of MSCs under inflammatory conditions, MSCs derived from the alveolar bones of Ccrl2-KO mice and WT mice were extracted, and total cellular RNA was extracted after 2 days of osteogenic induction under TNFα-induced inflammation, and carried out RNA-Seq to identify the potential mechanism by which Ccrl2 regulates osteogenic-related signals.
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Project description:Autonomic neuronal dysfunction is associated with heart failure (HF). Here, we report that targeted vagal nerve stimulation (VNS) using optogenetics attenuates cardiac remodelling and HF induced by pressure overload. Unbiased approaches revealed that VNS decreased the proportion of the Ccrl2+ macrophage subset, which derived from myeloid monocytes and exhibited a distinct tumour necrosis factor-alpha (TNFα)-responsive, pro-hypertrophic, and profibrotic signature. Elimination of Ccrl2+ macrophages prevented cardiac remodelling and HF. Functional characterisation by Ccrl2+ macrophage-specific overexpression or global genetic loss of α7 nicotinic acetylcholine receptor (α7nAChR) highlighted its crucial contribution to VNS-mediated cardioprotection. Mechanistically, activation of α7nAChR inhibited the TNFα responsiveness through upregulated expression of the transcription factor NRF2. Cardiac Ccrl2+ macrophages and TNFα-responsive proteins were positively correlated with cardiac remodelling and dysfunction in humans. Finally, an α7nAChR agonist effectively blocked the development of HF. These results suggest that the vagal neuroimmune axis modulates heart failure and is a promising target for treatment.
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Project description:Autonomic neuronal dysfunction is associated with heart failure (HF). Here, we report that targeted vagal nerve stimulation (VNS) using optogenetics attenuates cardiac remodelling and HF induced by pressure overload. Unbiased approaches revealed that VNS decreased the proportion of the Ccrl2+ macrophage subset, which derived from myeloid monocytes and exhibited a distinct tumour necrosis factor-alpha (TNFα)-responsive, pro-hypertrophic, and profibrotic signature. Elimination of Ccrl2+ macrophages prevented cardiac remodelling and HF. Functional characterisation by Ccrl2+ macrophage-specific overexpression or global genetic loss of α7 nicotinic acetylcholine receptor (α7nAChR) highlighted its crucial contribution to VNS-mediated cardioprotection. Mechanistically, activation of α7nAChR inhibited the TNFα responsiveness through upregulated expression of the transcription factor NRF2. Cardiac Ccrl2+ macrophages and TNFα-responsive proteins were positively correlated with cardiac remodelling and dysfunction in humans. Finally, an α7nAChR agonist effectively blocked the development of HF. These results suggest that the vagal neuroimmune axis modulates heart failure and is a promising target for treatment.
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Project description:The goal of this study was to determine expression profiles of microRNAs (miRNAs) in whole cell extracts of human bone marrow-derived mesenchymal stem/stromal cells (MSCs) as well as in MSCs during osteogenic differentiation. MicroRNAs are epigenetic regulators that commonly function by targeting specific mRNAs resulting in suppression of protein expression and modulation of a number of cellular pathways. This experiment is part of a larger study analyzing the expression of mitochondria-associated miRNAs in MSCs during osteogenesis that we recently submitted to GEO (Series GSE134946). Here, the same three human MSC lines were used in this study, under the same osteogenic induction conditions, to generate expression profiles of miRNAs present in whole cell extracts. A standard in vitro osteogenesis assay system was used to differentiate MSCs toward the osteoblast lineage.Purified whole cell extracts were obtained from MSCs or from MSCs at specific time points of osteogenic induction. RNA was isolated from whole cell extracts and then biotin-labeled in preparation for microRNA array (Affymetrix miRNA array 4.0). Array data was analyzed to generate information on most abundantly-expressed miRNAs in non-induced MSCs as well as in MSCs at set time points (day 3, 7, or 14) of osteogenic induction. Information on significantly differentially-expressed miRNAs during osteogenesis (comparing day 0 with either day 3, 7 or 14) was also obtained.
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Project description:Autonomic neuronal dysfunction is associated with heart failure (HF). Here, we report that targeted vagal nerve stimulation (VNS) using optogenetics attenuates cardiac remodelling and HF induced by pressure overload. Unbiased approaches revealed that VNS decreased the proportion of the Ccrl2+ macrophage subset, which derived from myeloid monocytes and exhibited a distinct tumour necrosis factor-alpha (TNFα)-responsive, pro-hypertrophic, and profibrotic signature. Elimination of Ccrl2+ macrophages prevented cardiac remodelling and HF. Functional characterisation by Ccrl2+ macrophage-specific overexpression or global genetic loss of α7 nicotinic acetylcholine receptor (α7nAChR) highlighted its crucial contribution to VNS-mediated cardioprotection. Mechanistically, activation of α7nAChR inhibited the TNFα responsiveness through upregulated expression of the transcription factor NRF2. Cardiac Ccrl2+ macrophages and TNFα-responsive proteins were positively correlated with cardiac remodelling and dysfunction in humans. Finally, an α7nAChR agonist effectively blocked the development of HF. These results suggest that the vagal neuroimmune axis modulates heart failure and is a promising target for treatment.
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Project description:Autonomic neuronal dysfunction is associated with heart failure (HF). Here, we report that targeted vagal nerve stimulation (VNS) using optogenetics attenuates cardiac remodelling and HF induced by pressure overload. Unbiased approaches revealed that VNS decreased the proportion of the Ccrl2+ macrophage subset, which derived from myeloid monocytes and exhibited a distinct tumour necrosis factor-alpha (TNFα)-responsive, pro-hypertrophic, and profibrotic signature. Elimination of Ccrl2+ macrophages prevented cardiac remodelling and HF. Functional characterisation by Ccrl2+ macrophage-specific overexpression or global genetic loss of α7 nicotinic acetylcholine receptor (α7nAChR) highlighted its crucial contribution to VNS-mediated cardioprotection. Mechanistically, activation of α7nAChR inhibited the TNFα responsiveness through upregulated expression of the transcription factor NRF2. Cardiac Ccrl2+ macrophages and TNFα-responsive proteins were positively correlated with cardiac remodelling and dysfunction in humans. Finally, an α7nAChR agonist effectively blocked the development of HF. These results suggest that the vagal neuroimmune axis modulates heart failure and is a promising target for treatment.
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Project description:The goal of this study was to determine expression profiles of mitochondria-associated microRNAs (mitomiR) in human bone marrow-derived mesenchymal stem/stromal cells (MSCs) as well as in MSCs during osteogenic differentiation. MicroRNAs are epigenetic regulators that commonly function by targeting specific mRNAs resulting in suppression of protein expression. In addition to their location in the cytosol, microRNAs have also been found in other sub-cellular compartments including the mitochondria. While some studies suggest that mitomiRs may affect mitochondrial function, research on mitomiRs is still in its infancy. To date, there is no information on mitomiR expression in MSCs or osteoblasts. A standard in vitro osteogenesis assay system was used to differentiate MSCs toward the osteoblast lineage. Purified mitochondrial extracts were obtained from MSCs or from MSCs at specific time points of osteogenic induction. RNA was isolated from mitochondrial extracts and then biotin-labeled in preparation for microRNA array (Affymetrix miRNA array 4.0). Array data was analyzed to generate information on most abundantly-expressed mitomiRs in non-induced MSCs as well as in MSCs at set time points (day 3, 7, or 14) of osteogenic induction. Information on significantly differentially-expressed mitomiRs during osteogenesis (comparing day 0 with either day 3, 7 or 14) was also obtained.
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Project description:The intriThe intricate balance between MSCs differentiation to osteoblasts or adipocytes is finely regulated. To explore novel participating molecules, we screened for early-stage osteogenesis- or adipogenesis-based MSCs protein expression profile using TMT-based quantitative proteomic analysis. Protein annotation, hierarchical clustering, functional stratification, and protein-protein association assessments were performed. Moreover, two upregulated proteins, namely, FBLN2 and NPR3, were validated to participate in the osteogenic differentiation process of MSCs. Subsequently, we independently downregulated FBLN2 and NPR3 during 7 days of osteogenic differentiation, and conducted quantitative proteomics analysis to assess the differential protein regulation between knockdown and control cells. Based on gene ontology (GO) and network analyses, FBLN2 deficiency induced functional alterations associated with biological regulation and stimulus response, whereas, NPR3 deficiency induced functional alterations related to cellular and metabolic processes, and so on. These results demonstrated that proteomics is still an effective tool for the comprehensive exploration of the MSCs differentiation process. cate balance between MSCs differentiation to osteoblasts or adipocytes is finely regulated. To explore novel participating molecules, we screened for early-stage osteogenesis- or adipogenesis-based MSCs protein expression profile using TMT-based quantitative proteomic analysis. Protein annotation, hierarchical clustering, functional stratification, and protein-protein association assessments were performed. Moreover, two upregulated proteins, namely, FBLN2 and NPR3, were validated to participate in the osteogenic differentiation process of MSCs. Subsequently, we independently downregulated FBLN2 and NPR3 during 7 days of osteogenic differentiation, and conducted quantitative proteomics analysis to assess the differential protein regulation between knockdown and control cells. Based on gene ontology (GO) and network analyses, FBLN2 deficiency induced functional alterations associated with biological regulation and stimulus response, whereas, NPR3 deficiency induced functional alterations related to cellular and metabolic processes, and so on. These results demonstrated that proteomics is still an effective tool for the comprehensive exploration of the MSCs differentiation process.
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