Balance macrophage polarization via cell synthesis of apoptotic bodies in hydrogel microspheres
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA996561 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25346043_1.fastq.gz | Fastqsanger.gz | |||
| SRR25346043_2.fastq.gz | Fastqsanger.gz | |||
| SRR25346044.fastq.gz | Fastqsanger.gz | |||
| SRR25346044_1.fastq.gz | Fastqsanger.gz | |||
| SRR25346044_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 19 |
Similar Datasets
Project description:Maintaining the homeostasis of immune ecological niches such as macrophages is essential for skin regeneration. In this study, apoptotic bodies (ABs) with intact bioactive substances of ADSC were constructed by biosynthesis. Further, injectable apoptotic bodies-GelMA microspheres (ABs@GMS) were constructed by microfluidics to maintain the homeostasis of the immune ecological niche in trauma, and inhibit the secretion of argininosuccinate synthetase 1 (ASS1) by ABs-induced downregulated JAK/STAT1 signaling pathway. Consequently, the macrophages’ polarization and inflammatory response were balanced in the wound with promoted angiogenesis. This ABs-functionalized microsphere slowly released biosynthetic apoptotic vesicles that expressed C1q, C3b and other surface "eat me" signals. These vesicles can be directly recognized, phagocytosed and degraded by macrophages, and allow scavenger cells to give meaning to cell death. In vitro, ABs@GMS balanced the JAK/STAT signaling pathway in a form of positive communication from dead to living cells via apoptotic vesicles. In vivo, ABs@GMS balanced the polarization of macrophages and increased the expression of α-smooth muscle actin. In conclusion, ABs synthesized by ADSC can balance traumatic immune disorders and restore homeostasis of the wound immune microenvironment, which would be a highly promising material for macrophage-mediated wound repair.
2023-11-30 | GSE237758 | GEO
Project description:he dynamic balance of hypoxia and oxidative stress constitutes the oxygen-related microenvironment in injured tissues. Oxygen homeostasis is highly variable; therefore, it is not a therapeutic target for injured tissue repair. We found an enrichment and extensive apoptosis of mesenchymal stem cells (MSCs) infused intravenously in the wound microenvironment with co-existing hypoxia and oxidative stress. Apoptotic bodies (ABs), generated from in situ apoptosis, significantly promotes angiogenesis. We improved the derivation pathway of ABs by simulating oxygen homeostasis in injured tissues, with cobalt chloride-induced hypoxia or hydrogen peroxide-induced oxidative stress in MSCs. Oxygen-related environmental stressed ABs, derived from environments of hypoxic and oxidative stress, were identified and loaded onto hydrogel microspheres for accurate regulation of endothelial cells (ECs) vascularization. These ABs directly targeted ECs; oxidative stress ABs (Oxi-ABs) have a 2.5- and 4-fold higher tube-forming ability than hypoxic and normoxic ABs, respectively. miRNA microarray analysis revealed that different oxygen-stressed ABs deliver similar miRNAs, which leads to the broad upregulation of EC phosphokinase activity. Finally, local delivery of Oxi-ABs-loaded hydrogel microspheres promotes wound healing. Oxi-ABs-loaded hydrogel microspheres achieved controlled AB release, targeting EC by reducing the consumption of early inflammatory cells and adapting to the proliferative phase of wound healing. Thus, the biogenerated apoptotic bodies responding to oxygen-related environmental stress can target ECs to promote vascularization.
2024-01-01 | GSE240216 | GEO
Project description:Adhesive and injectable hydrogel microspheres for NRF2-mediated periodontal bone regeneration
| PRJNA1158710 | ENA
Project description:For comparing the molecular profiling of the biological effect of the MMS and MMS-CY microspheres on the PDLSCs, the RNA-seq was performed to identify the gene change.
2025-01-15 | GSE276691 | GEO
Project description:We have been interested whether peripheral tolerance can be restored by vaccination with antigen-presenting cells (APCs) loaded with apoptotic bodies. Dendritic cells (DCs) are powerful APCs that have a critical role in the initiation and progression of autoimmunity. We previously demonstrated that DCs loaded with apoptotic islet cells prevents experimental type 1 diabetes (T1D), an autoimmune disease caused by beta-cell destruction. The goal of this study is to characterize the molecular changes on gene expression -transcriptome- occurring in these DCs pulsed with apoptotic bodies. Cells from four different genetically identical NOD (Non-Obese Diabetic) mice were used to obtain DCs. DCs were loaded with apoptotic bodies from NIT-1 cell line (insulinoma from NOD mice). Unloaded DCs were used as control in four paired experiments. Moreover, transcriptome from NIT-1 apoptotic bodies was determined. Mouse Gene 1.0 ST Arrays from Affymetrix (28,853 genes) were hybridized and genes with a p-value <= 0.002, adjusted p-value <= 0.08 and fold change (FC) >= 1.38 were considered upregulated, and genes with FC <= -1.37 were considered downregulated. Results demonstrate that apoptotic cells engulfment promotes molecular changes in DCs towards tolerogenic features. Gene expression profile of DCs from NOD mice that captured NIT-1 apoptotic bodies showed a downregulation of genes involved in antigen presentation and differential expression of cytokine, chemokine, natural immunity and immunoregulation genes together with the presence of specific transcripts for islet autoantigens. Molecular changes of DCs caused by the uptake of apoptotic bodies are key factors to induce antigen-specific peripheral tolerance.
2013-05-22 | E-MEXP-3374 | biostudies-arrayexpress
Project description:A reliable suspension-based platform for scaling engineered cardiac tissue (ECT) production from human induced pluripotent stem cells (hiPSCs) is crucial for regenerative therapies. Here, we compared the production and functionality of ECTs formed using our scaffold-based, engineered tissue microsphere differentiation approach with those formed using the prevalent scaffold-free aggregate platform. We utilized a microfluidic system for the rapid (1 million cells/min), high density (30, 40, 60 million cells/ml) encapsulation of hiPSCs within PEG-fibrinogen hydrogel microspheres. HiPSC laden-microspheres and aggregates underwent suspension-based cardiac differentiation in chemically defined media. In comparison to aggregates, microspheres maintained consistent size and shape initially, over time, and within and between batches. Initial size and shape coefficients of variation for microspheres were eight and three times lower, respectively, compared to aggregates. On day 10, microsphere cardiomyocyte (CM) content was 27% higher and the number of CMs per initial hiPSC was 250% higher than for aggregates. Contraction and relaxation velocities of microspheres were four and nine times higher than those of aggregates, respectively. Microsphere contractile functionality also improved with culture time, whereas aggregate functionality remained unchanged. Additionally, microspheres displayed improved β-adrenergic signaling responsiveness and uniform calcium transient propagation. Transcriptomic analysis revealed that while both microspheres and aggregates demonstrated similar gene regulation patterns associated with cardiomyocyte differentiation, heart development, cardiac muscle contraction, and sarcomere organization, the microspheres exhibited more pronounced transcriptional changes over time. Taken together, these results highlight the capability of the microsphere platform for scaling up biomanufacturing of ECTs in a suspension-based culture platform.
2024-10-16 | GSE276741 | GEO
Project description:Apoptosis plays a pivotal role in embryogenesis and postnatal cell homeostasis, involving DNA or subcellular fragmentation, and shedding of small membranous microvesicles termed apoptotic bodies (AB). Following DNA damage, hypoxia, or vascular injury, the chemokine CXCL12 has been implicated in the recruitment of progenitor cells for tissue regeneration through its receptor CXCR4 and in mechanisms counteracting apoptosis. Whether AB deliver alarm signals for regenerative responses to neighbouring cells beyond recruitment or eat-me signals for phagocytes and relevance to diseases with abundant apoptosis, eg atherosclerosis, remains unknown. Here we show that endothelial cell-derived AB are generated during diet-induced atherosclerosis and can be transferred to recipient endothelial or smooth muscle cells to induce functional expression of CXCL12. This is mediated through miRNA-126 enriched in AB, which acts by silencing RGS16 translation and unlocking CXCR4 to unleash an auto-regulatory feedback loop inducing CXCL12. Injection of AB promoted mobilization and incorporation of progenitor cells, reducing diet-induced atherosclerosis in apolipoprotein E-deficient mice, and local transfer of microRNA-126 inhibited collar-induced arterial plaque formation. This was associated with increased smooth muscle content but decreased macrophage and apoptotic cell content, all features of plaque stability. Our data identify a new mechanism, by which AB confer microRNA-126 as a paracrine alarm messenger to enhance CXCR4 signals and CXCL12 expression, thereby limiting or repairing vascular damage. This adds to the important functions of microRNAs in health and disease and may extend to progenitor cell recruitment during other forms of tissue repair or homeostasis. AB were isolated from supernatants of apoptotic, serum-starved human umbilical vein endothelial cells (HUVECs) by sequential centrifugation steps. Total RNA was isolated from AB or HUVECs and microRNA was purified using the mirVanaTM miRNA Isolation Kit (Ambion). microRNA obtained from 10 µg of total RNA was labeled using the mirVanaTM miRNA Labeling Kit (Ambion) and fluorescent Cy3 (Molecular Probes), and hybridized to the Ambion mirVanaTM miRNA Bioarray (1566 v.1). Hybridized mirVana miRNA Bioarrays were scanned and quantified by using ImaGene 5.5.4 (Bio Discovery). Resulted signal intensities were background corrected and then normalized using variance stabilization normalization. (Huber, 2002).
2010-08-31 | E-GEOD-12696 | biostudies-arrayexpress
Project description:Apoptosis plays a pivotal role in embryogenesis and postnatal cell homeostasis, involving DNA or subcellular fragmentation, and shedding of small membranous microvesicles termed apoptotic bodies (AB). Following DNA damage, hypoxia, or vascular injury, the chemokine CXCL12 has been implicated in the recruitment of progenitor cells for tissue regeneration through its receptor CXCR4 and in mechanisms counteracting apoptosis. Whether AB deliver alarm signals for regenerative responses to neighbouring cells beyond recruitment or eat-me signals for phagocytes and relevance to diseases with abundant apoptosis, eg atherosclerosis, remains unknown. Here we show that endothelial cell-derived AB are generated during diet-induced atherosclerosis and can be transferred to recipient endothelial or smooth muscle cells to induce functional expression of CXCL12. This is mediated through miRNA-126 enriched in AB, which acts by silencing RGS16 translation and unlocking CXCR4 to unleash an auto-regulatory feedback loop inducing CXCL12. Injection of AB promoted mobilization and incorporation of progenitor cells, reducing diet-induced atherosclerosis in apolipoprotein E-deficient mice, and local transfer of microRNA-126 inhibited collar-induced arterial plaque formation. This was associated with increased smooth muscle content but decreased macrophage and apoptotic cell content, all features of plaque stability. Our data identify a new mechanism, by which AB confer microRNA-126 as a paracrine alarm messenger to enhance CXCR4 signals and CXCL12 expression, thereby limiting or repairing vascular damage. This adds to the important functions of microRNAs in health and disease and may extend to progenitor cell recruitment during other forms of tissue repair or homeostasis.
2010-08-31 | GSE12696 | GEO
Project description:Profiling of mRNA, lncRNA and circRNA in Apoptotic Bodies during Osteoclastogenesis by RNA-seq
| PRJNA546562 | ENA
Project description:Increasing evidences are revealing the important biological functions of apoptotic bodies (ABs). Here we identified the proteomic profiles of ABs from osteoclasts of distinct differentiation stages and investigated the potential functions. ABs were isolated from apoptotic bone marrow macrophages (BMMs), pre-osteoclasts (pOCs) or mature osteoclasts (mOCs). Proteomic signature analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) followed by bioinformatic analysis showed that proteomic signatures of ABs exhibited high similarities with the parental cells. Functionally, pOC-ABs induced endothelial progenitor cell (EPC) differentiation and increased CD31hiEmcnhi endothelial cell formation in a murine bone defect model via PDGF-BB. mOC-ABs induced mesenchymal stem cell (MSC) osteogenic differentiation and promoted bone formation via RANKL reverse signaling. Together, our results mapped the detailed proteomic landscapes of osteoclast derived ABs and demonstrated that the biological functions of ABs are largely inherited from corresponding parental cells, suggesting a novel extended intercellular regulation after cell apoptosis.
2021-09-08 | PXD017245 | Pride