scholarly journals Degradation of Elastin in Emphysema Is Exacerbated by Peptidyl Arginine Deiminase Activity

2020 ◽  
Author(s):  
M. Murphy ◽  
R. Alshuhoumi ◽  
J. McDonnell ◽  
D. Hunt ◽  
N.G. McElvaney ◽  
...  
Keyword(s):  
Arginine Deiminase ◽  
Peptidyl Arginine Deiminase

scholarly journals Silver Nanoparticles Induce Neutrophil Extracellular Traps Via Activation of PAD and Neutrophil Elastase

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 317
Author(s):  
HanGoo Kang ◽  
Jinwon Seo ◽  
Eun-Jeong Yang ◽  
In-Hong Choi
Keyword(s):  
Silver Nanoparticles ◽  
Neutrophil Elastase ◽  
Mammalian Cells ◽  
Antimicrobial Properties ◽  
Neutrophil Extracellular Traps ◽  
Arginine Deiminase ◽  
Human Neutrophils ◽  
Extracellular Traps ◽  
Peptidyl Arginine Deiminase ◽  
Key Factor

Silver nanoparticles (AgNPs) are widely used in various fields because of their antimicrobial properties. However, many studies have reported that AgNPs can be harmful to both microorganisms and humans. Reactive oxygen species (ROS) are a key factor of cytotoxicity of AgNPs in mammalian cells and an important factor in the immune reaction of neutrophils. The immune reactions of neutrophils include the expulsion of webs of DNA surrounded by histones and granular proteins. These webs of DNA are termed neutrophil extracellular traps (NETs). NETs allow neutrophils to catch and destroy pathogens in extracellular spaces. In this study, we investigated how AgNPs stimulate neutrophils, specifically focusing on NETs. Freshly isolated human neutrophils were treated with 5 or 100 nm AgNPs. The 5 nm AgNPs induced NET formation, but the 100 nm AgNPs did not. Subsequently, we investigated the mechanism of AgNP-induced NETs using known inhibitors related to NET formation. AgNP-induced NETs were dependent on ROS, peptidyl arginine deiminase, and neutrophil elastase. The result in this study indicates that treatment of 5 nm AgNPs induce NET formation through histone citrullination by peptidyl arginine deiminase and histone cleavage by neutrophil elastase.

scholarly journals Autoimmunity to peptidyl arginine deiminase type 4 precedes clinical onset of rheumatoid arthritis

2010 ◽  
Vol 62 (9) ◽  
pp. 2633-2639 ◽  
Author(s):  
Jason R. Kolfenbach ◽  
Kevin D. Deane ◽  
Lezlie A. Derber ◽  
Colin I. O'Donnell ◽  
William R. Gilliland ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Arginine Deiminase ◽  
Peptidyl Arginine Deiminase ◽  
Clinical Onset

scholarly journals Porphyromonas gingivalis Peptidyl Arginine Deiminase Can Modulate Neutrophil Activity via Infection of Human Dental Stem Cells

2018 ◽  
Vol 10 (4) ◽  
pp. 264-278 ◽  
Author(s):  
Katja Kriebel ◽  
Cathleen Hieke ◽  
Robby Engelmann ◽  
Jan Potempa ◽  
Brigitte Müller-Hilke ◽  
...  
Keyword(s):  
Stem Cells ◽  
Porphyromonas Gingivalis ◽  
Chronic Inflammatory Disease ◽  
Arginine Deiminase ◽  
Dental Stem Cells ◽  
Host Proteins ◽  
Phenotypic Changes ◽  
Peptidyl Arginine Deiminase ◽  
Immune Imbalance ◽  
Follicle Stem Cells

Periodontitis (PD) is a widespread chronic inflammatory disease in the human population. Porphyromonas gingivalis is associated with PD and can citrullinate host proteins via P. gingivalis peptidyl arginine deiminase (PPAD). Here, we hypothesized that infection of human dental follicle stem cells (hDFSCs) with P. gingivalis and subsequent interaction with neutrophils will alter the neutrophil phenotype. To test this hypothesis, we established and analyzed a triple-culture system of neutrophils and hDFSCs primed with P. gingivalis. Mitogen-activated pathway blocking reagents were applied to gain insight into stem cell signaling after infection. Naïve hDFSCs do not influence the neutrophil phenotype. However, infection of hDFSCs with P. gingivalis prolongs the survival of neutrophils and increases their migration. These phenotypic changes depend on direct cellular contacts and PPAD expression by P. gingivalis. Active JNK and ERK pathways in primed hDFSCs are essential for the phenotypic changes in neutrophils. Collectively, our results confirm that P. gingivalis modifies hDFSCs, thereby causing an immune imbalance.

Modulation of Peptidyl Arginine Deiminase 2 and Implication for Neurodegeneration

2006 ◽  
Vol 31 (12) ◽  
pp. 1063-1071 ◽  
Author(s):  
Sanjoy K. Bhattacharya ◽  
Manjunatha B. Bhat ◽  
Hidenari Takahara
Keyword(s):  
Arginine Deiminase ◽  
Peptidyl Arginine Deiminase

scholarly journals Neutrophil Extracellular Traps Promote the Development of Intracranial Aneurysm Rupture

Hypertension ◽  
2021 ◽  
Author(s):  
Masaaki Korai ◽  
James Purcell ◽  
Yoshinobu Kamio ◽  
Kazuha Mitsui ◽  
Hajime Furukawa ◽  
...  
Keyword(s):  
Intracranial Aneurysm ◽  
Interleukin 1 ◽  
Neutrophil Extracellular Traps ◽  
Aneurysm Rupture ◽  
Arginine Deiminase ◽  
Intercellular Adhesion Molecule ◽  
Necrosis Factor Alpha ◽  
Extracellular Traps ◽  
Peptidyl Arginine Deiminase ◽  
Aneurysm Wall

Potential roles for neutrophils in the pathophysiology of intracranial aneurysm have long been suggested by clinical observations. The presence of neutrophil enzymes in the aneurysm wall has been associated with significant increases in rupture risk. However, the mechanisms by which neutrophils may promote aneurysm rupture are not well understood. Neutrophil extracellular traps (NETs) were implicated in many diseases that involve inflammation and tissue remodeling, including atherosclerosis, vasculitis, and abdominal aortic aneurysm. Therefore, we hypothesized that NETs may promote the rupture of intracranial aneurysm, and that removal of NETs can reduce the rate of rupture. We employed both pharmacological and genetic approaches for the disruption of NETs and used a mouse model of intracranial aneurysm to investigate the roles of NETs in the development of intracranial aneurysm rupture. Here, we showed that NETs are detected in human intracranial aneurysms. Both global and granulocyte-specific knockout of peptidyl arginine deiminase 4 (an enzyme essential for NET formation) reduced the rate of aneurysm rupture. Pharmacological blockade of the NET formation by Cl-amidine also reduced the rate of aneurysm rupture. In addition, the resolution of already formed NETs by deoxyribonuclease was effective against aneurysm rupture. Inhibition of NETs formation with Cl-amidine decreased mRNA expression of proinflammatory cytokines (intercellular adhesion molecule 1 (ICAM-1), interleukin 1 beta (IL-1β), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor alpha (TNF-α)) in cerebral arteries. These data suggest that NETs promote the rupture of intracranial aneurysm. Pharmacological removal of NETs, by inhibition of peptidyl arginine deiminase 4 or resolution of already-formed NETs, may represent a potential therapeutic strategy for preventing aneurysmal rupture.

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