Exosomes from MSC facilitate diabetic wound healing by promoting angiogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA812774 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18218765_1.fastq.gz | Fastqsanger.gz | |||
| SRR18218765_2.fastq.gz | Fastqsanger.gz | |||
| SRR18218766_1.fastq.gz | Fastqsanger.gz | |||
| SRR18218766_2.fastq.gz | Fastqsanger.gz | |||
| SRR18218767_1.fastq.gz | Fastqsanger.gz |
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Project description:Mesenchymal stem cell (MSC)-derived exosomes had been reported to be a prospective candidate in accelerating diabetic wound healing. Hence, this study intended to explore whether exosomes originating from the human umbilical cord MSC (hucMSC) could display a superior proangiogenic effect on diabetic wound repair and its underlying molecular mechanism.
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Project description:We here addressed the question whether the unique capacity of mesenchymal stromal/stem cells (MSCs) to re-establish tissue homeostasis depends on their potential to sense pathogen associated molecular pattern (PAMP) and, in consequence, mount an adaptive response in the interest of tissue repair. After injection of MSCs which had been primed with the bacterial wall component LPS into murine wounds, an unexpected acceleration of healing occurred, clearly exceeding that of non-primed MSCs. This correlates with a fundamental reprogramming of the transcriptome in LPS treated MSCs as deduced from RNA-seq analysis and its validation. A network of genes mediating the adaptive response through the TLR-4 pathway responsible for neutrophil activation (GCP- 2, ENA-78, IL-1β IL-8) and MSC protection (SOX6) profoundly contributes to enhanced wound healing. In fact, silencing of either TRL-4, or IRAK3, a downstream effector of TRL-4, or SOX6 suppressed wound healing most likely due to suppression of neutrophil extracellular trap formation and suppression of the enhanced microbicidal release of reactive oxygen species (ROS), key features of neutrophil activation. This previously unreported results uncover SOX6 which protects MSCs at the wound site from enhanced oxidative stress. This unprecedented findings hold substantial promise to refine current MSC-based therapies for difficult-to-treat wounds.
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Project description:Therapeutic use of mesangial stem cells (MSCs) for tissue repair, including heart, has great potential. MSCs from multiple sources, including those derived from human umbilical matrix, namely Wharton's jelly, may serve as a resourceful candidate. Even after more than a decade, low engraftment efficacy of MSCs, in vivo, remains a limitation which requires in-depth understanding of the mechanisms and factors involved to facilitate a better and clinically relevant outcome. We recently hypothesized and demonstrated that the sex hormone – 17-beta estradiol (E2) – facilitates protective processes within the cardiovascular system by modulating MSC function, in vitro. Here, using a proteomic approach, we investigated the angiogenic potential of MSCs in vivo and the modulatory actions of E2 on mechanisms involved in tissue repair (potentially post-ischemic injury). Employing an in vivo approach with an ovariectomized (OVX) mice model, we evaluated the effects of E2 on MSC-induced angiogenesis using Matrigel plug assay.
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Project description:Macrophages are progenitors of osteoclasts, but macrophages themselves also regulates bone metabolism. Macrophages mediate not only bone formation by osteoblasts in physiological conditions, but also regeneration after fracture. However, the mechanisms how macrophages control bone formation and regeneration remain unclear. Here we demonstrate that liposome-encapsulated Clodronate (Clod-lip) model with targeted depletion of phagocytic macrophages exhibits impaired angiogenesis of type H vessels, which couple angiogenesis and osteogenesis, in mouse cortical bone defect model by drill-hole injury. Additionaly, we identify Tgfbi (encoding TGF, beta-induced protein), Plau (encoding uPA), and Tgfb1 (encoding TGF-β1) as genes of macrophage-secreted factors mediating angiogenesis and wound healing by RNA-seq analysis. These mRNAs were highly expressed in bone marrow-derived macrophages among bone cells by qRT-PCR. Finally, we show that treatment with uPA inhibitor or TGF-β Receptor I, Receptor II inhibitor impaired bone regeneration after injury, confirming importance of uPA and TGF-β1 for bone repair. Therefore, we proposed that these factors may be potential for therapeutic targets for delayed union, or non-union patients. Our findings reveal a novel mechanism of bone regeneration mediated by macrophages.
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Project description:Search for macrophage-derved factors related to angiogenesis and wound healing
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Project description:Although the paracrine effects of mesenchymal stem/stromal cells (MSCs) have been recognized as crucial mediators of their regenerative effects on tissue repair, the potential of MSC secretomes as effective substitutes for cellular therapies remains underexplored. In this study, we compared MSCs from the human dermis (DSCs) and adipose tissue (ASCs) with their secretomes regarding their efficacy for skin wound healing using a translationally-relevant murine model. Proteomic analysis revealed that while there was a substantial overlap in protein composition between DSC and ASC secretomes, specific proteins associated with wound healing and angiogenesis were differentially expressed. Despite a similar angiogenic potential in vivo, DSC- and ASC-secretomes were found to be less effective than cells in accelerating wound closure and promoting tissue remodeling. Overall, secretome-treated groups showed intermediary results between cells and control (empty scaffold) treated groups. These findings highlight that although secretomes possess therapeutic potential, their efficacy might be limited compared to cellular therapies. This study contributes to the growing understanding of MSC secretomes, emphasizes the need for further protocol optimization, and offers insights into their potential applications in regenerative medicine.
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Project description:Exosomes derived from mesenchymal stem cells (MSCs) have shown to have effective application prospects in the medical field, but exosome yield is very low. The production of exosome mimetic vesicles (EMVs) by continuous cell extrusion leads to more EMVs than exosomes, but whether the protein compositions of MSC-derived EMVs (MSC-EMVs) and exosomes (MSC-exosomes) are substantially different remains unknown. The purpose of this study was to conduct a comprehensive proteomic analysis of MSC-EMVs and MSC-exosomes and to simply explore the effects of exosomes and EMVs on wound healing ability. This study provides a theoretical basis for the application of EMVs and exosomes.In this study, EMVs from human umbilical cord MSCs (hUC MSCs) were isolated by continuous extrusion, and exosomes were identified after hUC MSC ultracentrifugation. A proteomic analysis was performed, and 2,315 proteins were identified. The effects of EMVs and exosomes on the proliferation, migration and angiogenesis of human umbilical vein endothelial cells (HUVECs) were evaluated by cell counting kit-8, scratch wound, Transwell and tubule formation assays. A mouse mode was used to evaluate the effects of EMVs and exosomes on wound healing . Bioinformatics analyses revealed that 1,669 proteins in both hUC MSC-EMVs and hUC MSC-exosomes play roles in retrograde vesicle-mediated transport and vesicle budding from the membrane. The 382 proteins unique to exosomes participate in extracellular matrix organization and extracellular structural organization, and the 264 proteins unique to EMVs target the cell membrane. EMVs and exosomes can promote wound healing and angiogenesis in mice and promote the proliferation, migration and angiogenesis of HUVECs.
2022-08-11 | PXD033899 | Pride
Project description:The interaction between neurogenesis and angiogenesis after traumatic brain injury is a complex and dynamic process. To resolve this, we chose the zebrafish model organism for studying brain wound healing via systems biology approach. Transcriptome microarray data and histological analysis of injured fish were sampled at different time points during recovery process. Time-course microarray data following wound healing of zebrafish were obtained. From this set of data, we constructed two intracellular protein–protein interaction (PPI) networks for the traumatic brain injury healing mechanism.
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