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LOX inhibition (BAPN treatment) attenuates satellite cell differentiation

ABSTRACT: LOX inhibition (BAPN treatment) attenuates satellite cell differentiation

PROVIDER: PRJNA612783 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11310279.fastq.gz	Fastqsanger.gz
	SRR11310280.fastq.gz	Fastqsanger.gz
	SRR11310281.fastq.gz	Fastqsanger.gz
	SRR11310282.fastq.gz	Fastqsanger.gz
	SRR11310283.fastq.gz	Fastqsanger.gz

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LOX inhibition (BAPN treatment) attenuates satellite cell differentiation

Project description:Integration of extracellular matrix (ECM)-derived cues into transcriptional programs is essential primarily in rapidly morphing environments such as regenerating tissues. Here we demonstrate that Lysyl oxidase (Lox), known for its ECM modifying activities, primarily collagen crosslinking and fibronectin matrix assembly, also directly regulates transcription factor (TF) localization. Using genetic and pharmacological strategies, we highlight a novel intracellular role for Lox in myogenic progenitors essential for muscle regeneration. We show that Lox interacts with, and directly oxidizes, Vestigial-Like 3 (Vgll3), a transcriptional co-activator acting with Mef2 and TEF TFs. This enzymatic activity is required for Vgll3 cytoplasmic to nuclear translocation in regulation of myogenic differentiation. Our work highlights a novel mechanism for TF sub-cellular localization and suggests a mechanism for integrating ECM organization with transcriptional output during myogenic differentiation. Modulating this integration mechanism could affect the balance between ECM organization and cell differentiation and serve as a basis for novel therapeutic strategies targeting fibrotic pathologies.

2020-03-17 | GSE147007 | GEO

Inhibition of endothelial Notch signaling attenuates inflammation

Project description:Inhibition of endothelial Notch signaling attenuates inflammation

| PRJNA339936 | ENA

A highly potent bi-thiazole inhibitor of LOX rewires collagen architecture and enhances chemoresponse in triple-negative breast cancer

Project description:Matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI) data investigating changes in extracellular matrix/collagen architecture of mouse tumor tissue in response to LOX inhibition. Sample Key: Vehicle, Doxo (Chemotherapy drug), 6403 (LOX inhibitor), Combo (Doxo + LOX inhibitor)

2024-07-25 | PXD052657 | Pride

Fibrostenotic phenotype of fibroblasts in Crohn's disease is dependent on tissue stiffness and reversed by LOX inhibition

Project description:The results of this study indicate that stenotic fibroblasts exhibit an aberrant response to tissue stiffness with reduced MMP activity, leading to a perpetuous vicious circle of ever more fibrosis formation. Altering the microenvironment by LOX inhibition increases MMP activity and decreases ECM contraction, resulting in a potential anti-fibrotic agent for Crohn’s disease.

2018-08-09 | GSE90607 | GEO

Effect of LOX-PP on the gene expression profile of the A673 cell line (Ewing sarcoma)

Project description:In this study we show that lysyl oxidase (LOX), an enzyme involved in maintaining structural integrity of the extracellular matrix, is expressed at low levels in Ewing sarcoma cells and primary tumors and is downregulated by the EWS/FLI1 oncoprotein characteristic of these tumors. Using a doxycycline inducible system to restore LOX expression in an Ewing sarcoma derived cell line, we show that LOX displays tumor suppressor activities. Interestingly, we show that the tumor suppressor activity resides in the propeptide domain of LOX (LOX-PP), an N-terminal domain produced by proteolytic cleavage during the physiological processing of LOX. Finally, we show that LOX-PP inhibits ERK/MAPK signalling pathway, and that many pathways involved in cell cycle progression were significant deregulated by LOX-PP, providing a mechanistic explanation to the cell proliferation inhibition observed upon LOX-PP expression. In summary, our observations indicate that deregulation of the LOX gene participates in Ewing sarcoma development and identify LOX-PP as a new therapeutic target for one of the most aggressive paediatric malignancies. These findings suggest that therapeutic strategies based in the administration of LOX propeptide or functional analogues could be useful in the treatment of this devastating paediatric cancer.

2013-12-31 | GSE46407 | GEO

LOX-1-dependent transcriptional regulation after oxidized LDL (OxLDL) treatment of human aortic endothelial cells.

Project description:LOX-1 is the primary endothelial receptor for oxidized LDL in endothelial cells and plays a role in the development of atherosclerosis. Expression profiling was carried out on samples from HAECT cells over-expressing either LOX-1 or GFP control and treated with or without OxLDL over a time course of 2, 6, 12 and 24 Hours. The goal of the study was to identify genes expression changes activated by OxLDL binding to LOX-1 at several different time points.

2009-10-07 | GSE13139 | GEO

Effect of LOX-PP on the gene expression profile of the A673 cell line (Ewing sarcoma)

2013-12-31 | E-GEOD-46407 | biostudies-arrayexpress

Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos

Project description:Conditional ablation of Ezh2 in the neural crest lineage results in loss of the neural crest-derived mesenchymal derivatives. In this data sheet we determine gene expression analysis in Ezh2lox/lox and Wnt1Cre Ezh2lox/lox in E11.5 mouse BA1 cells. Conditional ablation of Ezh2 in the neural crest lineage was achieved by crossing Wnt1creEzh2lox/wt mice with Ezh2lox/lox mouse lines. We analyzed a total of 6 samples including 3 biological replicates from Ezh2lox/lox embryos and 3 biological replicates from Wnt1cre Ezh2lox/lox embryos.

2013-11-09 | E-GEOD-52220 | biostudies-arrayexpress

Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos

2013-11-09 | GSE52220 | GEO

Activation of Piezo1-mediated mechanotransduction by LOX promotes neuronal ferroptosis leading to HIBD and discovery of LOX inhibitor TA

Project description:Neonatal hypoxic-ischemic brain damage (HIBD) is initiated by perinatal asphyxia, leading to brain injury triggered by reduced blood and oxygen flow, resulting in neurological impairments such as cerebral palsy, epilepsy, cognitive deficits, and behavioral disorders.Recent insights collectively suggest the important roles of lysyl oxidase (LOX) in the pathological processes of several acute and chronic neurological diseases, but the molecular regulatory mechanisms in HIBD remain elusive.In this study, we found through the study of HIBD rat models and the oxygen-glucose deprivation/re-oxygenation (OGD/R) cell models that LOX significantly increased after HIBD or OGD/R. RNA seq results showed a significant increase in piezo1 after primary neuron OGD/R, and iron death data was also enriched. Moreover, inhibiting LOX or piezo1 can rescue neuronal ferroptosis and further improve cognitive function in rats. In addition, we also found that traumatic acid can inhibit the enzyme activity of LOX and improve a series of pathological features of neuronal damage caused by increased LOX.

2024-09-25 | GSE270560 | GEO

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