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Mechanism for Human Adipose Stem Cell-Derived Exosomes' Therapeutic Effect on Chronic Liver Fibrosis

ABSTRACT: Mechanism for Human Adipose Stem Cell-Derived Exosomes' Therapeutic Effect on Chronic Liver Fibrosis

PROVIDER: PRJNA821315 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18531063_1.fastq.gz	Fastqsanger.gz
	SRR18531063_2.fastq.gz	Fastqsanger.gz
	SRR18531064_1.fastq.gz	Fastqsanger.gz
	SRR18531064_2.fastq.gz	Fastqsanger.gz
	SRR18531065_1.fastq.gz	Fastqsanger.gz

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Mechanism for Human Adipose Stem Cell-Derived Exosomes' Therapeutic Effect on Chronic Liver Fibrosis

Project description:The goal of this study was to understand the effect of human adipose stem cell and its derived exosomes on mouse chronic liver fibrosis. After eight weeks of intraperitoneal injection of CCl4, we treated 200μl PBS, normal human adipose stem cell (1×106/200μl PBS), human adipose stem cell-derived exosomes(250μg/200μl PBS) once a week for 4 weeks. Then the livers were collected and isolated RNA for RNA-sequencing to explore alterations in mRNA expression between different treatments

2022-04-02 | GSE199732 | GEO

Exosomes Facilitate Therapeutic Targeting of STAT3 in Liver Fibrosis

Project description:Exosomes Facilitate Therapeutic Targeting of STAT3 in Liver Fibrosis

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Inhalation of Lung Spheroid Cell-Secreted Factors and Exosomes Promotes Therapeutic Lung Repair in Rodent Models of Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a fatal form of interstitial lung disease in which persistent injury results in scar tissue formation. As fibrosis thickens, the lung tissue becomes stiff and losses the ability to facilitate gas exchange and provide cells with needed oxygen. Currently, IPF has few treatment options and no effective therapies, aside from lung transplant. Here we present a series of studies utilizing lung spheroid cell-derived conditioned media (LSC-CM) and exosomes (LSC-EXO) to treat different rodent models of lung injury and fibrosis. Inhalation treatment was given for seven consecutive days via a nebulizer for clinical relevance. Results revealed that LSC-CM and LSC-EXO treatments could attenuate and resolve bleomycin- and silica-induced fibrosis by reestablishing normal alveolar structure, decreasing collagen accumulation, and myofibroblast proliferation. In addition, LSC-CM and LSC-EXOs exhibited superior therapeutic benefits than their counterparts derived from bone marrow mesenchymal stem cells. LSC-CM and LSC-EXOs provide promising therapeutic options for pulmonary fibrosis.

2019-11-18 | GSE136263 | GEO

Exosomes derived from TREM-2 knocked-out macrophages alleviated renal fibrosis via HSPa1b/AKT pathway

Project description:Macrophages are recognized as the vital players in renal fibrosis, with a high degree of heterogeneity and plasticity, and triggering receptor expressed on myeloid cell-2(TREM-2) was highly expressed on macrophages and participated in the progression of tissue fibrosis. However, the mechanism by which TREM-2 mediate the progress of renal fibrosis is still unclear. Our study have found the exosomes derived from TREM-2 deficient (TREM-2-/-) macrophages could suppress the progression of fibrosis, showing a higher matrix metalloproteinase-9 (MMP-9) / tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) ration at protein level in secreted exosomes than exosomes from WT（wild type）macrophages in the fibrotic microenvironment. Besides, renal tubular epithelial cells (TECs) engulfed theses nanoscale vesicles, the expression of collagen I and α-smooth muscle actin (α-SMA) (fibrosis related marker) was obviously decreased. Through the RNA-seq, we found that TREM-2-/- macrophages upregulate the MMP-9/TIMP-1 ratio in its exosomes via HSPa1b/AKT pathway. Furthermore, it’s noteworthy that the renal fibrosis was effectively alleviated in the obstructed kidney from mice received a renal pelvis injection of adeno associated virus (AAV-shTREM-2) containing the sequence of silencing TREM-2. However, VER-155008 (inhibitor of HSPa1b) and Ly294002 (inhibitor of AKT) reversed this effect. Moreover, polyclonal antibodies against TREM-2 also effectively relieved the UUO-induced renal fibrosis. Above all, we have validated that the knocking down TREM-2 expression can inhibit the progression of renal fibrosis through a macrophage exosome-dependent pathway in vitro and vivo. Hence, our finding suggest TREM-2 is potential therapeutic target for CKD.

2024-11-29 | GSE262665 | GEO

Cystic Fibrosis disease Urine exosomes

Project description:Cystic Fibrosis is a life limiting disease due to mutations in the Cystic Fibrosis Conductance Gene Regulator (CFTR). This is associated with a multiorgan disease combining pancreatic insufficiency, chronic infected bronchopathy and production of a salty sweat. Increased survival of patients leads to observation of new complications, including proximal tubule transport dysfunctions with increased output of glucose, amino acids, phosphate, calcium, uric acid, and low Molecular Weight proteins, which ultimately triggers tubulo-interstitial injury and chronic kidney disease. (Jouret et al. 2007) Exosomes are membrane vesicles stemming from Multi-Vesicular Bodies. They reflect the biological state of the cell they stem from because they incorporate various bioactive molecules from their cell of origin, which can be transferred to target cells. They are therefore ideal biomarkers for early diagnosis, prediction of disease progression or response to treatment. Urinary exosomes have been largely investigated in kidney or urothelial diseases and exosomal proteins proved to be biomarkers reflecting renal cellular biology. We hypothetized that urinary exosomal proteins might be differentially expressed, according to the presence of the mutation in the CFTR gene and its correction. We analyzed urinary exosomes of patients with CF and healthy controls based on their protein content determined by high resolution mass spectrometry, in combination with Gene Set Enrichment Analysis. These results were compared to those obtained in exosomes collected in patients treated with CFTR modulators.

2021-03-29 | PXD018537 | Pride

miRNA profiles within lean and obese adipose tissue macrophages-derived exosomes

Project description:Small RNA deep sequencing analysis on the microRNA components within exosomes secreted from adipose tissue macrophages of lean and obese mice

2017-09-01 | GSE97652 | GEO

The effect of high or low fat diet on the miRNA composition of exosomes derived from adipose tissue

Project description:Exosomes are nanosized extracellular vesicles with lipid bilayer membranes and contain various contents, including lipids, miRNAs and proteins, all of which are widely involved in signaling pathways and genetic information processes. Exosomes derived from adipose tissues (AT-Exos) have been identified as a crucialmedium in the transmission of information from adipose tissue to itself and to other organs, including exosomes derived from inguinal white adipose tissue (iWAT-Exos), visceral white adipose tissue (vWAT-Exos) and brown adipose tissue (BAT-Exos). Here we reported that dietary conditions and tissue origins of exosome can affect the composition and function of miRNAs in AT-Exos, mainly including lipid metabolism and inflammatory signaling pathways associated with metabolic imbalance.

2024-04-25 | GSE264481 | GEO

The Hippo pathway links adipocyte plasticity to adipose tissue fibrosis

Project description:Fibrosis disrupts adipose tissue (AT) homeostasis in response to chronic caloric excess, exacerbating metabolic dysfunction. The molecular mechanisms linking adipocyte plasticity to AT fibrosis are largely unknown. Here we show that the Hippo pathway is coupled with TGFbeta signaling to orchestrate a functional adipocyte-to-myofibroblast transition in AT fibrosis. We found that Lats1/2-knockout adipocytes could dedifferentiate into DPP4+ progenitor cells and convert to DPP4- myofibroblasts upon TGFbeta stimulation. Macrophages recruited by CCL2 served as a major cell source of TGFbeta. YAP and TAZ, the Hippo downstream effectors, enhanced SMAD2 stability to promote fibrotic responses. Importantly, inhibition of YAP/TAZ activity in obese mice markedly relieved AT fibrosis and improved metabolic homeostasis. Together, our findings identify the Hippo pathway as a molecular switch in the initiation and development of AT fibrosis, implying it as a therapeutic target.

2022-08-11 | GSE184826 | GEO

Inhalation of Lung Spheroid Cell-Secreted Factors and Exosomes Promotes Therapeutic Lung Repair in Rodent Models of Pulmonary Fibrosis

Project description:Inhalation of Lung Spheroid Cell-Secreted Factors and Exosomes Promotes Therapeutic Lung Repair in Rodent Models of Pulmonary Fibrosis

| PRJNA561784 | ENA

LPS preconditioning enhances the therapeutic efficacy of MSC-derived exosomes in sepsis by altering miRNA expression profile

Project description:Studies have shown that stimulation of Mesenchymal stem cells (MSCs) with biophysical or biochemical cues could influence the contents and biological activities of subsequent MSC-derived exosomes. However, the underlying mechanisms have not been fully clarified. Here, we pretreated MSCs with lipopolysaccharide (LPS) and evaluated exosomes (LPS-Exo) therapeutic effects in sepsis. Analysis of exosomes activity revealed that LPS-Exo treatment improved sepsis to a greater extent than normal MSCs-derived exosomes (Exo). Further analysis revealed that LPS-Exo exert their protective effects mainly through RNA contents. Thus, we hypothesized that LPS preconditioning enhances the therapeutic efficacy of LPS-Exo in sepsis by altering miRNA expression profile.

2024-05-16 | GSE261810 | GEO

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