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Anti-CX3CL1 (fractalkine) monoclonal antibody attenuates lung and skin fibrosis in sclerodermatous graft-versus-host disease mouse model

ABSTRACT: Anti-CX3CL1 (fractalkine) monoclonal antibody attenuates lung and skin fibrosis in sclerodermatous graft-versus-host disease mouse model

PROVIDER: PRJNA944580 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23857011_1.fastq.gz	Fastqsanger.gz
	SRR23857011_2.fastq.gz	Fastqsanger.gz
	SRR23857012_1.fastq.gz	Fastqsanger.gz
	SRR23857012_2.fastq.gz	Fastqsanger.gz
	SRR23857013_1.fastq.gz	Fastqsanger.gz

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Anti-CX3CL1 (fractalkine) monoclonal antibody attenuates lung and skin fibrosis in sclerodermatous graft-versus-host disease mouse model

Project description:To assess the preclinical utility and functional mechanism of intraperitoneal anti-CX3CL1 mAb therapy in the skin and lung fibrosis, sclerodermatous chronic graft-versus-host disease (Scl-cGVHD) model mice were analyzed by RNA-sequencing assays.

2024-05-03 | GSE227285 | GEO

Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

Project description:Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

2021-09-15 | GSE161555 | GEO

Microarray of human primary CD16+ monocytes treated with fractalkine (CX3CL1) against untreated controls

Project description:This experiment is a part of the larger study on angiotensin II role in the upregulation of the CX3CL1 expression and its release in human first trimester placenta. CX3CL1 (or fractalkine) is chemokine involved in the pathogenesis of hypertension, which can be secreted by trophoblasts, initiating the cross talk with monocytes. Thus, we performed the microarray experiment to study the effects of recombinant human CX3CL1 on the transcriptome of human primary monocytes.

2019-02-08 | E-MTAB-7484 | biostudies-arrayexpress

The CX3CL1-CX3CR1 chemokine axis can contribute to tumor immune evasion and blockade with a novel CX3CR1 monoclonal antibody enhances responses to anti-PD-1 immunotherapy [CT26]

Project description:To investigate the imunoresistance programs regulated by the CX3CL1-CX3CR1 axis, we treated CT26 mouse tumor cell line with CX3CL1, CX3CL1 + IFN-γ, IFN-γ, and no treatment

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Adult cardiomyocytes treated with fractalkine (CX3CL1)

Project description:Background and Aims: It is known that inflammatory processes are activated in heart failure, but the regulation of cytokines and their role in the pathogenesis of the disease are not well understood. We have identified fractalkine as a possible novel mediator in HF development. To address this issue, we have performed microarray analysis of cardiomyocytes treated with different isoforms of fractalkine. Methods: Cardiomyocytes isolated from adult rat hearts and treated with different forms of fractalkine for 24 hours. Control cells were treated with BSA. Molecular alterations in myocardial tissue were measured by using cDNA microarrays. Molecular pathways affected were identified by the Ingenuity Pathway Analysis software. Results: Several molecular pathways were affected upon fractalkine stimulation of adult cardiomyocytes. Keywords: Fractalkines effect on cardiomyocytes

2008-02-01 | GSE7397 | GEO

Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

Project description:Fractalkine Antibody Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mice model

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Transcription profiling of mouse adult cardiomyocytes treated with fractalkine (CX3CL1)

2008-06-18 | E-GEOD-7397 | biostudies-arrayexpress

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Project description:Adult cardiomyocytes treated with fractalkine (CX3CL1)

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Back-signaling from CX3CL1 regulates neurogenesis during development and in the adult mouse

Project description:CX3CL1 was discovered as a chemokine, and is best known to function via interaction with its receptor CX3CR1. However, in this study, we report a unique role of CX3CL1 that is independent from this pathway. We show that CX3CL1 is naturally shedded by both α- and β-secretase. The membrane-anchored C-terminal fragment is further cleaved by γ-secretase to release the CX3CL1 intracellular domain (CX3CL1-ICD), which is translocated into the cell nucleus to control gene expression. Among the regulated genes, we noted prominent induction of TGFβ2/TGFβ3 signaling in cultured cells by CX3CL1-ICD. Mice overexpressing only the C-terminal fragment (Tg-CX3CL1-ct) strongly induced TGFβ3 expression, as evidenced by Western and RNAseq analyses. Phenotypically, Tg-CX3CL1-ct mice exhibited enhanced neurogenesis both during development and in adulthood. Enhanced adult neurogenesis was seen in both the subgranular zone and the subventricular zone. Together, we demonstrate that CX3CL1-ct has a back-signaling function by enhancing neurogenesis through TGFβ3 and other genes important for neurogenesis. Induction CX3CL1 back signaling may be a promising novel mechanism to replenish neuronal loss.

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