Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Peptidylarginine deiminase 4 deficiency improves elastase-induced formation of neutrophil extracellular traps and emphysema in mouse lung

ABSTRACT: Peptidylarginine deiminase 4 deficiency improves elastase-induced formation of neutrophil extracellular traps and emphysema in mouse lung

PROVIDER: PRJNA1200037 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31772844.fastq.gz	Fastqsanger.gz
	SRR31772845.fastq.gz	Fastqsanger.gz
	SRR31772846.fastq.gz	Fastqsanger.gz
	SRR31772847.fastq.gz	Fastqsanger.gz
	SRR31772848.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Peptidylarginine deiminase 4 deficiency improves elastase-induced formation of neutrophil extracellular traps and emphysema in mouse lung

Project description:Neutrophil extracellular traps (NETs) are associated with the extracellular release of nuclear chromatin decorated with cytoplasmic proteins. Excessive release of NETs has been reported in chronic lung diseases, including chronic obstructive pulmonary disease (COPD). However, the role of NETs in the pathogenesis of COPD remains unclear. Peptidylarginine deaminase 4 (PAD4) contributes to NET formation. Therefore, in an elastase (ELS)-induced emphysema mouse model, we examined the role of PAD4 using the Padi4 gene knockout (KO) mice. First, we confirmed that ELS induced NET formation in the lungs. Although PAD4 deficiency did not affect the cellular profile of bronchoalveolar lavage fluid (BALF), PAD4 deficiency suppressed ELS-induced neutrophil migration and NET expression in the parenchyma of the lung. Additionally, PAD4 deficiency ameliorated emphysema and apoptosis in lung cells. Finally, we examined the effects of PAD4 on comprehensive gene expression signatures using RNA sequencing. Enrichment analysis of the transcriptomic data revealed that the expression of several genes associated with COPD pathogenesis was altered in the KO mice. Overall, the results suggest that PAD4 deficiency improves NET formation and emphysema in the lungs; this pathway can be a potential therapeutic target for the treatment of COPD.

2025-06-04 | GSE284684 | GEO

Peptidylarginine deiminase 4 promotes the renal infiltration of neutrophils and exacerbates the TLR7 agonist-induced lupus mice

Project description:Peptidylarginine deiminase 4 (PAD4), encoded by PADI4, plays critical roles in the immune system. The pathological roles of PAD4 were investigated in lupus model mice. PAD4-regulated pathways were identified by RNA-sequencing of WT and Padi4 KO neutrophils.

2020-02-19 | GSE145422 | GEO

Presence of peptidylarginine deiminase in Porphyromonas gingivalis-related species

Project description:Presence of peptidylarginine deiminase in Porphyromonas gingivalis-related species

| PRJEB21305 | ENA

Examination of the role of peptidylarginine deiminase 2 (PAD2) in gene expression in MCF-7 breast cancer cells

2012-04-07 | GSE37087 | GEO

Examination of the role of peptidylarginine deiminase 2 (PAD2) in gene expression in MCF-7 breast cancer cells

Project description:To investigate the potential role of peptidylarginine deiminase 2 (PAD2) in gene expression, we created stable shRNA scrambled control and PAD2 knockdown MCF-7 breast cancer cell lines. After validating the specific knockdown of PAD2 at the mRNA and protein level, we utilized an Agilent microarray platform to compare the gene expression profile of the two cell lines to generate a candidate list of genes regulated by PAD2. Control and PAD2 knockdown cells were created by stably transfecting shRNA constructs into MCF-7 cells. Stable cells were selected using puromycin and knockdown validate at the mRNA and protein level. Microarray data represents 4 independent biological replicates contain control and PAD2 knockdown samples.

2012-04-06 | E-GEOD-37087 | biostudies-arrayexpress

Exploration of the genes affecting the compound acting against emphysema development in a mouse model of elastase-induced emphysema.

2016-08-24 | GSE85962 | GEO

Eosinophils promote lung emphysema via CTSL

Project description:Patients with chronic obstructive pulmonary disease (COPD) having higher blood eosinophil levels exhibit worse lung function and more severe emphysema, implying the potential role of eosinophils in emphysema development. However, the specific mechanism underlying eosinophil-mediated emphysema development is not fully elucidated. In this study, single-cell RNA sequencing was used to identify eosinophil subgroups in mouse models of asthma and emphysema and analyze their functions. Analysis of the accumulated eosinophils revealed differential transcriptomes between the mouse lungs of elastase-induced emphysema and ovalbumin-induced asthma., Eosinophil depletion alleviated elastase-induced emphysema. Notably, eosinophil-derived cathepsin L (CTSL) degraded the extracellular matrix (ECM), causing emphysema in the pulmonary tissue. Eosinophils were positively correlated with serum CTSL levels, which were increased in patients with emphysema than in those without emphysema. Collectively, these results suggest that CTSL expression in eosinophils plays an important role in ECM degradation and remodeling and is related to emphysema in patients with COPD. Therefore, eosinophil-derived CTSL may serve as a potential therapeutic target for patients with emphysema.

2023-10-17 | GSE237749 | GEO

Exploration of the genes affecting the compound acting against emphysema development in a mouse model of elastase-induced emphysema.

Project description:In a mouse model of elastase-induced emphysema, the effect of tetomilast against the emphysema development observed in C57BL/6J (C57) could be also detected in phosphodiesterase (PDE) 4D(+/+) but not in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) mice. Based on this result, we hypothesized that the difference in the efficacy of tetomilast among these strains of mice might result from the differences in the levels of the target molecules of tetomilast other than PDE4 in each mouse strain. To test this hypothesis, we used microarrays to compare the expression levels of genes in the lungs of each mouse strain. The expression profiling by array demonstrated that the levels of cyclin-dependent kinase inhibitor 1 (CDKN1a) in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) were higher than those in C57 and PDE4D(+/+). Total RNAs were extracted from the lungs from naÃ¯ve mice in each strain [C57, PDE4B(+/+), PDE4B(-/-), PDE4D(+/+), and PDE4D(-/)], and were used for microarray. In comparison with the expression levels of genes in C57, we retrieved the genes which expressed at the same levels in PDE4D(+/+), and at the different levels in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-).

2016-08-24 | E-GEOD-85962 | biostudies-arrayexpress

Testosterone deficiency altered mortality and the expression profile of protease inhibitors in an elastase-induced mouse model of emphysema

Project description:To evaluate the effect of testosterone on the pathophysiology of COPD, we created porcine pancreas elastase (PPE)-induced emphysema mouse model in sham or orchiectomized (ORX) mice [sham/PBS, sham/PPE, ORX/PBS, and ORX/PPE]. We performed microarray analysis to compare the gene expression levels in the lungs of each mice group. The results demonstrated that the levels of genes encoding protease inhibitor activity in ORX/PPE mice were lower than those in sham/PPE mice.

2023-06-24 | GSE153148 | GEO

Lung genes modification in elastase-induced emphysema following in utero nicotine exposure

Project description:Lung genes modification in elastase-induced emphysema following in utero nicotine exposure

| PRJNA704966 | ENA