A5021506859- Retinal Diseases and Treatments
- Nitric Oxide and Endothelin Effects
- Neuroinflammation and Neurodegeneration Mechanisms
- Traumatic Brain Injury and Neurovascular Disturbances
- Retinal Development and Disorders
- Retinopathy of Prematurity Studies
- Amino Acid Enzymes and Metabolism
- Retinal and Optic Conditions
- Glaucoma and retinal disorders
- Neurological Complications and Syndromes
- Adenosine and Purinergic Signaling
- Metabolism and Genetic Disorders
- Polyamine Metabolism and Applications
- Anesthesia and Neurotoxicity Research
- Mitochondrial Function and Pathology
- Intraoperative Neuromonitoring and Anesthetic Effects
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cannabis and Cannabinoid Research
- Immune cells in cancer
- Acute Kidney Injury Research
- Advanced Glycation End Products research
- Infectious Encephalopathies and Encephalitis
- Phosphodiesterase function and regulation
- Mast cells and histamine
- Acute Ischemic Stroke Management
Cairo University
2019-2025
University of Arkansas for Medical Sciences
2022-2025
Augusta University Health
2016-2022
Augusta University
2014-2021
Charlie Norwood VA Medical Center
2016-2021
Discovery Institute
2015-2021
Benha University
2021
Georgia Regents Medical Center
2015-2016
Veterans Health Administration
2016
We have recently found that diabetes-induced premature senescence of retinal endothelial cells is accompanied by NOX2-NADPH oxidase-induced increases in the ureohydrolase enzyme arginase 1 (A1). Here, we used genetic strategies to determine specific involvement A1 cell senescence. knockout mice and wild type were rendered diabetic with streptozotocin (ECs) exposed high glucose or transduced adenovirus overexpress for these experiments. ABH [2(S)-Amino-6-boronohexanoic acid] was inhibit...
Abstract Retinal ischemia is a major cause of visual impairment and blindness involved in various disorders including diabetic retinopathy, glaucoma, optic neuropathies retinopathy prematurity. Neurovascular degeneration common feature these pathologies. Our lab has previously reported that the ureahydrolase arginase 2 (A2) ischemic retinopathies. Here, we are introducing A2 as therapeutic target to prevent neurovascular injury after retinal ischemia/reperfusion (I/R) insult. Studies were...
Abstract The lack of effective therapies to limit neurovascular injury in ischemic retinopathy is a major clinical problem. This study aimed examine the role ureohydrolase enzyme, arginase 1 (A1), retinal ischemia-reperfusion (IR) injury. A1 competes with nitric oxide synthase (NOS) for their common substrate l -arginine. A1-mediated -arginine depletion reduces (NO) formation by NOS leading vascular dysfunction when endothelial involved but prevents inflammatory inducible involved. Studies...
Department of Pharmacology and Toxicology, College Medicine, University Arkansas for Medical Sciences, Little Rock, AR, USA (Fouda AY, Shosha E) Clinical Pharmacy, Faculty Cairo University, Cairo, Egypt *Correspondence to: Abdelrahman Y. Fouda, PhD, [email protected]. This is an open access journal, articles are distributed under the terms Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License (http://creativecommons.org/licenses/by-nc-sa/4.0/), which allows others to remix,...
Our previous studies have implicated expression of the mitochondrial isoform arginase enzyme 2 (A2) in neurovascular injury during ischemic retinopathies. The aim this study was to characterize specific involvement A2 retinal following optic nerve crush (ONC). To accomplish this, wild-type (WT) or knockout (A2-/-) mice were subjected ONC injury. contralateral eye served as sham control. Quantitative RT-PCR and western blot used evaluate mRNA protein expression. Retinal ganglion cell (RGC)...
Retinal ischemic disease is a major cause of vision loss. Current treatment options are limited to late-stage diseases, and the molecular mechanisms initial insult not fully understood. We have previously shown that deletion mitochondrial arginase isoform, 2 (A2), limits neurovascular injury in models retinopathy. Here, we investigated involvement A2-mediated alterations dynamics function pathology. used wild-type (WT), global A2 knockout (A2KO-) mice, cell-specific mice subjected retinal...
Dysfunction of retinal neurons is a major cause vision impairment in blinding diseases that affect children and adults worldwide. Cellular damage resulting from polyamine catabolism has been demonstrated to be player many neurodegenerative conditions. We have previously shown inhibition oxidase (PAO) using MDL 72527 significantly reduced neurodegeneration cell death signaling pathways hyperoxia-mediated retinopathy. In the present study, we investigated impact PAO limiting model NMDA...
Current therapies for treatment of proliferative retinopathy focus on retinal neovascularization (RNV) during advanced disease and can trigger adverse side-effects. Here, we have tested a new strategy limiting neurovascular injury promoting repair early-stage disease. We recently shown that with stable, pegylated drug form the ureohydrolase enzyme arginase 1 (A1) provides neuroprotection in acute models ischemia/reperfusion injury, optic nerve crush, ischemic stroke. Now, determined effects...
Abstract The enzyme arginase 1 (A1) hydrolyzes the amino acid arginine to form L-ornithine and urea. Ornithine is further converted polyamines by ornithine decarboxylase (ODC) enzyme. We previously reported that deletion of myeloid A1 in mice exacerbates retinal damage after ischemia/reperfusion (IR) injury. Furthermore, treatment with protects against IR injury wild-type mice. PEG-A1 also mitigates exaggerated inflammatory response knockout (KO) macrophages vitro. Here, we sought identify...
Diabetic retinopathy (DR) is the leading cause of vision loss in working age adults. Understanding retinal metabolic response to circulating high glucose levels diabetic patients critical for development new therapeutics treat DR. Measuring function using Seahorse analyzer a promising technique investigate effect hyperglycemia on glycolysis and mitochondrial respiration. Here, we analyzed young old control mice. We also compared expression key glycolytic enzymes between two groups. The XF...
Abstract Ischemia-induced retinopathy is a hallmark finding of common visual disorders including diabetic (DR) and central retinal artery vein occlusions. Treatments for ischemic retinopathies fail to improve clinical outcomes the design new therapies will depend on understanding underlying disease mechanisms. Histone deacetylases (HDACs) are an enzyme class that removes acetyl groups from histone non-histone proteins, thereby regulating gene expression protein function. HDACs have been...
Central retinal artery occlusion (CRAO) is an ocular emergency that results from acute blockage of the blood supply to retina and leads a sudden vision loss. Other forms ischemic retinopathies include diabetic retinopathy (DR), which involves chronic ischemia remains leading cause blindness in working-age adults. This study first conduct proteomic analysis aqueous humor (AH) patients with CRAO comparative using vitreous (VH) samples DR.
Cellular senescence has been considered as a contributing factor to diabetes related complications. The present study was undertaken evaluate involvement of the ureahydrolase enzyme arginase 1 (A1) in diabetes‐induced vascular and bone marrow cells. Studies were performed using retinas cells from wild type (WT) A1 knockout diabetic control mice cultured bovine retinal endothelial (BRE) treated with high glucose or transduced 1. senescence, indicated by increases senescence‐associated beta...
Objective Our group has previously shown that the ureahydrolyase mitochondrial isoenzyme, arginase 2 (A2) is involved in ischemia reperfusion (I/R)‐induced retinal neurovascular degeneration. We found A2 homozygous deletion significantly protected against necroptosis, degeneration, thinning, and impairment of function. Interestingly, our also a link between hypoxia‐induced increases impaired angiogenesis endothelial cells. The cytosolic isoform 1 (A1) was not affected which suggests distinct...
Objective Our group has previously shown that degeneration of the retinal microvasculature after ischemia/reperfusion (I/R) injury is mediated through increased expression mitochondrial isoform arginase, arginase 2 (A2). In contrast, cytosolic isoform, 1 (A1) involved in impairment endothelial cell (EC)‐dependent vasorelaxation. We have global deletion A2 limits I/R‐induced vascular whereas EC‐specific A1 prevents diabetes‐induced EC dysfunction. However, specific involvement as yet unknown....
Purpose We have discovered that treatment with PEGylated arginase 1 (PEG‐A1) protects against inflammation and neurovascular injury in retina models of ischemia/reperfusion (IR) whereas deletion myeloid A1 exacerbates the damage. also found PEG‐A1 limits LPS‐induced macrophages (MΦ) by reducing inducible nitric oxide synthase (iNOS)‐derived nitrative oxidative stress promoting a reparative MΦ phenotype. This project aimed to elucidate mechanisms underlying protective effects A1. Arginase...
This study was conducted to evaluate the impact of stocking density on behavioral patterns, growth performance, blood hormones, and carcass quality Sasso broilers within 60 days rearing cycle.A total number 150 one day old unsexed (first generation) chicks were allocated randomly according their 3 groups 10,13 15 birds per m 2 in different floor spaces5, 3.8, 3.3 respectively.Growth performance patterns estimated throughout period.Blood samples for cortisol thyroid hormones estimation...