A5080444742- PARP inhibition in cancer therapy
- Asthma and respiratory diseases
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Ion Channels and Receptors
- Immune Cell Function and Interaction
- NF-κB Signaling Pathways
- Inflammasome and immune disorders
- Immune Response and Inflammation
- IL-33, ST2, and ILC Pathways
- Cell death mechanisms and regulation
- Coronary Interventions and Diagnostics
- Pediatric health and respiratory diseases
- Lipoproteins and Cardiovascular Health
- Cancer, Lipids, and Metabolism
- Cell Adhesion Molecules Research
- Inflammatory mediators and NSAID effects
- Antimicrobial Resistance in Staphylococcus
- Atherosclerosis and Cardiovascular Diseases
- Dermatology and Skin Diseases
- Trace Elements in Health
- Cytokine Signaling Pathways and Interactions
- Aldose Reductase and Taurine
- Whipple's Disease and Interleukins
- COVID-19 Clinical Research Studies
- Protein Kinase Regulation and GTPase Signaling
Panjab University
2015-2024
Louisiana State University Health Sciences Center New Orleans
2007-2016
University of New Orleans
2016
Stanley Foundation
2011-2016
Louisiana Cancer Research Center
2015
Louisiana State University
2007-2015
Southern University at New Orleans
2014
Molina Center for Energy and the Environment
2011
Mie University
2010
Institute of Pharmacology
2009
Abstract The role of NF-κB in the expression inflammatory genes and its participation overall process chronic diseases acute tissue injury are well established. We others have demonstrated a critical involvement poly(ADP-ribose) polymerase (PARP)-1 during inflammation, part, through relationship with NF-κB. However, mechanism by which PARP-1 affects activation has been elusive. In this study, we show that inhibition gene knockout, knockdown, or pharmacologic blockade prevented p65 nuclear...
Poly(ADP-ribose) polymerase (PARP) was suggested to play a role in endothelial dysfunction that is associated with number of cardiovascular diseases. We hypothesized PARP may an important atherogenesis and its inhibition attenuate atherosclerotic plaque development experimental model atherosclerosis.Using mouse (apolipoprotein E [ApoE](-/-)) high-fat diet-induced atherosclerosis, we demonstrate association between cell death oxidative stress-associated DNA damage activation within plaques....
Abstract The role of inducible NO synthase (iNOS) in allergic airway inflammation remains elusive. We tested the hypothesis that iNOS plays different roles during acute versus chronic inflammation. Acute and mouse models OVA-induced were used to conduct study. showed deletion was associated with a reduction eosinophilia, mucus hypersecretion, IL-5 IL-13 production upon protocol. Such protection completely abolished Interestingly, pulmonary fibrosis observed wild-type mice under protocol...
To cite this article: Datta R, Naura AS, Zerfaoui M, Errami Y, Oumouna Kim H, Ju J, Ronchi VP, Haas AL, Boulares AH. PARP-1 deficiency blocks IL-5 expression through calpain-dependent degradation of STAT-6 in a murine asthma model. Allergy 2011; 66: 853–861. Background: We recently showed that poly(ADP-ribose)polymerase-1 (PARP-1) may play role allergen (ovalbumin)-induced airway eosinophilia, potentially specific effect on production. also reported while replenishment promotes reversal...
Cordycepin has been shown to interfere with a myriad of molecular processes from RNA elongation kinase activity, and prevents numerous inflammatory in animal models. Here we show mouse model LPS-induced acute lung injury that cordycepin airway neutrophilia via robust blockade expression several genes, including the adhesion molecule ICAM-1 VCAM-1, cytokine/chemokine MCP-1, MIP-1α, MIP-2 KC, chemokine receptor CXCR2. Such appears be related severe reduction TNF-α expression. Interestingly, an...
An important portion of asthmatics do not respond to current therapies. Thus, the need for new therapeutic drugs is urgent. We have demonstrated a critical role PARP in experimental asthma. Olaparib, inhibitor, was recently introduced clinical trials against cancer. The objective present study examine efficacy olaparib blocking established allergic airway inflammation and hyperresponsiveness similar those observed human asthma animal models disease. used ovalbumin (OVA)-based mouse primary...
Abstract Airway inflammation induced by reactive oxygen species-mediated activation of redox-sensitive transcription factors is the hallmark asthma, a prevalent chronic respiratory disease. In various cellular and animal models, we have recently demonstrated that, in response to multiple stimuli, aldose reductase (AR) regulates inflammatory signals mediated NF-κB. Because NF-κB-mediated major characteristic asthma pathogenesis, investigated effect AR inhibition on NF-κB markers models using...
Our laboratory established a role for poly(ADP-ribose)polymerase (PARP) in asthma. To increase the clinical significance of our studies, it is imperative to demonstrate that PARP actually activated human asthma, examine whether inhibitor approved testing such as olaparib blocks already-established chronic asthma traits response house dust mite (HDM), true allergen, mice and drug modulates cluster differentiation type 4 (CD4+) T-cell function. conduct study, lung specimens peripheral blood...
Despite the reported role of poly(ADP-ribose) polymerase (PARP) in asthma inflammation, its contribution during remodeling is not clearly known. The main aim current investigation was to examine potential olaparib, a pharmacological inhibitor PARP against airway using an ovalbumin (OVA)-based murine model chronic asthma. results demonstrated that post-challenge olaparib treatment (5 mg/kg i.p., 30 min after OVA exposure) for six weeks (3 days/week) attenuates mucus production, and collagen...