Purpose: To determine whether the mechanical stretching renders modulation of the peptidyl arginine deiminase 2 (PAD2) expression in cultured astrocytes.
Methods: Isolated rat brain astrocytes were subjected to mechanical stretching using a glass bead set-up and polyethylene set-up with or without immobilization. Activity assays and ELISA were performed to detect PAD2 expression. Protein deimination levels in the cells were measured using an anti-citrulline ELISA. PAD2 expression in cells subjected to mechanical stretching was compared with controls. Astrocytes were also subjected to pressure treatment and compared to control cells for PAD2 expression and deimination levels.
Results: Astrocytes subjected to mechanical stretching with or without immobilization showed elevated PAD2 expression. Pressure treatment of astrocytes (25-100 mmHg) also resulted in elevated PAD2 expression and deimination.
Conclusion: These results suggest mechanical stretching induced PAD2 expression and consequent protein deimination.
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http://dx.doi.org/10.1080/02713680802447113 | DOI Listing |
Int Immunopharmacol
December 2024
Advanced Clinical Biosystems Research Institute, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Advanced Clinical Biosystems Research Institute, Precision Biomarker Laboratories, Cedars Sinai Medical Center, Los Angeles, CA, USA. Electronic address:
Objective: This study aimed to investigate the tumorigenic role and regulatory pathways of peptidyl arginine deiminase 2 (PAD-2) in A549 lung cancer cells following treatment with small interfering RNA (PADI-2 siRNA) or the pharmacological pan-PAD inhibitor BB-Cl amidine.
Materials And Methods: A549 lung cancer cells were treated with PADI-2 siRNA to knock down PADI-2 expression or with BB-Cl amidine to inhibit PAD2 activity. The effects on cell proliferation, migration, invasion, and cell cycle phases were assessed.
Biomed Pharmacother
November 2024
Advanced Clinical Biosystems Research Institute, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Advanced Clinical Biosystems Research Institute, Precision Biomarker Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address:
Background: Dilated cardiomyopathy (DCM) is characterized by enlarged, weakened heart ventricles due to chronic fibrosis. Dysfunctional senescent myofibroblasts and excessive citrullination have been implicated in fibrotic diseases. Peptidylarginine deiminases (PADs) are involved in the citrullination of ECM proteins.
View Article and Find Full Text PDFClin Exp Immunol
November 2024
Department of Pediatrics, Division of Infectious Diseases and Immunology, Guerin Children's at Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Kawasaki disease (KD) is the leading cause of acquired heart disease in children. While circulating neutrophils are increased and activated during acute KD, it is unclear whether neutrophils and neutrophil extracellular traps (NETs) contribute to the pathogenesis of KD. Peptidylarginine deiminase 4 (PAD4), an enzyme involved in protein citrullination and essential for NETs formation, is implicated in the pathogenesis of various diseases.
View Article and Find Full Text PDFInt J Mol Sci
August 2024
Department of Public Health and Pediatric Sciences, Medical School, University of Turin, 10124 Turin, Italy.
Protein expression is regulated through multiple mechanisms, including post-translational modifications (PTMs), which can alter protein structure, stability, localization, and function. Among these, citrullination stands out due to its ability to convert arginine residues into citrulline, altering protein charge and mass. This modification is catalyzed by calcium-dependent protein arginine deiminases (PADs), enzymes implicated in various inflammatory diseases.
View Article and Find Full Text PDFClin Exp Rheumatol
August 2024
Division of Rheumatology, Department of Internal Medicine, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul, Republic of Korea.
Objectives: To evaluate the role of Fcγ receptors (FcγR) and peptidyl arginine deiminase (PAD) in anti-citrullinated protein antibody (ACPA)-induced fibroblast-like synoviocytes (FLSs)-mediated osteoclastogenesis in patients with rheumatoid arthritis (RA).
Methods: FLSs and peripheral blood mononuclear cells were collected from patients with RA. We stimulated RA-FLS with ACPA (100 ng/ml) with and without anti-cluster of differentiation (CD)32a/CD64 (FcγRIIA/FcγRI) antibody and PAD-2/4 inhibitors.
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