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Chondroprotective functions of neutrophil-derived extracellular vesicles via promoting the production of secreted frizzled related protein 5 in cartilage [SFRP5]

ABSTRACT: Chondroprotective functions of neutrophil-derived extracellular vesicles via promoting the production of secreted frizzled related protein 5 in cartilage [SFRP5]

PROVIDER: PRJNA1130401 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29662200_1.fastq.gz	Fastqsanger.gz
	SRR29662200_2.fastq.gz	Fastqsanger.gz
	SRR29662201_1.fastq.gz	Fastqsanger.gz
	SRR29662201_2.fastq.gz	Fastqsanger.gz
	SRR29662202_1.fastq.gz	Fastqsanger.gz

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Chondroprotective functions of neutrophil-derived extracellular vesicles via promoting the production of secreted frizzled related protein 5 in cartilage

Project description:Chondroprotective functions of neutrophil-derived extracellular vesicles via promoting the production of secreted frizzled related protein 5 in cartilage

| PRJNA1130388 | ENA

Chondroprotective functions of neutrophil-derived extracellular vesicles via promoting the production of secreted frizzled related protein 5 in cartilage

Project description:Neutrophil extracellular vesicles (EVs) are known to play a protective role in arthritic joints by suppressing inflammation and cartilage degeneration. In the current study, we investigated the functional characteristics of EVs derived from stimulated neutrophils and their protective effects in cartilage repair in vitro. We first optimized the stimulation conditions of neutrophils that led to production of EVs with chondroprotective function. To understand this protective mechanism, EVs from TGF-β-stimulated neutrophils were added to stimulated chondrocytes with IL-1β, and their responses were examined by bulk-RNA analysis.

2024-11-26 | GSE271169 | GEO

Chondroprotective functions of neutrophil-derived extracellular vesicles via promoting the production of secreted frizzled related protein 5 in cartilage [SFRP5]

2024-11-26 | GSE271171 | GEO

Chondroprotective functions of neutrophil-derived extracellular vesicles by promoting the production of secreted frizzled-related protein 5 in cartilage.

Project description:BackgroundOsteoarthritis (OA) is the most common degenerative joint disease characterized by cartilage degradation and various degrees of inflammation in the synovium. Growing evidence highlights that neutrophil extracellular vesicles (EVs) play a protective role in arthritic joints by promoting the resolution of inflammation and the synthesis of proteoglycans in cartilage. However, this homeostatic function is dependent on the activation state of neutrophils and the surrounding environment/tissues. Hence, we explored the chondroprotective functions of neutrophil-derived EVs under different stimulation conditions and the underlying molecular mechanism.MethodsHuman blood-derived neutrophils, murine bone marrow-derived neutrophils, C-28I2 cells and primary chondrocytes were used. Neutrophils were stimulated with different cytokines, and their EVs were isolated for chondrocyte stimulation and further subjected to RNA-sequencing analysis. Two experimental murine OA models were used, and the treatment was performed by intraarticular injections.ResultsConditioned medium from neutrophils stimulated with TGF-β (N-β) had the greatest inhibitory effect on the expression of catabolic factors in stimulated chondrocytes. These protective effects were not impaired when conditioned medium of N-β from AnxA1-deficient mice was used. Consistent with these results, EVs isolated from N-β significantly reduced the expression of catabolic factors in stimulated chondrocytes. Bulk RNA-seq analysis revealed that secreted frizzled-related protein 5 (SFRP5) is upregulated in N-β-EV-stimulated chondrocytes. Furthermore, recombinant SFRP5 treatment significantly reduced the expression of catabolic factors in vitro and catabolic process in experimental murine OA models.ConclusionsThe current study emphasizes the potential therapeutic application of neutrophils in OA and provides new knowledge on the molecular mechanisms underlying their function.

| S-EPMC11603793 | biostudies-literature

Neutrophil extracellular traps mediate articular cartilage damage and enhance the immunogenicity of cartilage components in rheumatoid arthritis

Project description:This study invesigates the effects of neutrophil extracellular traps (NETs) on articular cartilage degredation and resulting autoimmune responses in rheumatoid arthritis.

2020-08-10 | GSE150466 | GEO

Secreted-frizzled-related protein 5 modulates calcium handling in human iPSC-cardiomyocytes

Project description:Secreted-frizzled-related protein 5 modulates calcium handling in human iPSC-cardiomyocytes

| PRJNA1001988 | ENA

Secreted-frizzled-related protein 5 modulates calcium handling in human iPSC-cardiomyocytes

Project description:End-stage heart failure caused by myocardial injury is a leading cause of death in the developed world, with high prevalence and poor prognosis. Current therapies focus on attenuating cardiac remodeling after a cardiovascular event such as myocardial infarction or pressure overload, but no therapy is currently available to halt or reverse disease progression. Recent studies have suggested a cardioprotective function of the Wnt5a inhibitor secreted frizzled-related protein 5 (SFRP5) in preventing adverse cardiac remodeling. However, until now, the underlying molecular mechanisms of SFRP5 treatment in the human heart are not well understood. In this study, we investigated the mechanistic and functional consequences of SFRP5 by establishing knockout and overexpression models in human iPSC-derived cardiomyocytes. Transcriptome profiling and deep pathway analysis revealed an involvement of SFRP5 in the regulation of calcium handling, cardiac contraction, and apoptosis. Functional analysis of iPSC-cardiomyocytes by live-cell calcium imaging confirmed the regulatory role of SFRP5 on calcium homeostasis. Our study uncovered a novel role of SFRP5 as a modulator of calcium handling, providing a deeper molecular understanding of the cardioprotective role of SFRP5 in the human heart.

2023-08-04 | GSE240053 | GEO

Neutrophil extracellular traps mediate articular cartilage damage and enhance the immunogenicity of cartilage components in rheumatoid arthritis

Project description:Neutrophil extracellular traps mediate articular cartilage damage and enhance the immunogenicity of cartilage components in rheumatoid arthritis

| PRJNA632502 | ENA

Secreted Frizzled-Related Protein 5 is Downregulated in Obesity and Promotes β-Cell Proliferation [30 days]

Project description:Obesity is associated with an increase in β-cell mass in response to the rising demand for insulin. β-cell plasticity is essential to maintaining glucose homeostasis, however, the cellular and molecular mechanisms by which β-cell mass is regulated remain poorly understood. Recently, we described the existence of a crosstalk between the peripancreatic adipose tissue and β-cells as a novel mechanism that participates in the regulation of β-cell plasticity. Here, we identify the secreted frizzled-related protein (Sfrp) 5 as down-regulated in the pancreatic islets of obese rats as well as in the pancreatic islets of human obese patients. Our results demonstrate that the silencing of Sfrp5 induces an increase in β-cell proliferation, which we correlate with the activation of Wnt signaling and of the MAPK and PI3 kinase pathways. Together, these findings expand our understanding of the mechanisms underlying β-cell proliferation under conditions of obesity. Furthermore, this study opens new insights into the specific targeting of Sfrp5 as a novel therapeutic strategy for balancing β-cell mass.

2014-10-10 | GSE44046 | GEO

Secreted Frizzled-Related Protein 5 is Downregulated in Obesity and Promotes β-Cell Proliferation [10 days]

2014-10-10 | GSE44045 | GEO