A5005128517- Heme Oxygenase-1 and Carbon Monoxide
- Acute Kidney Injury Research
- Neonatal Health and Biochemistry
- Autophagy in Disease and Therapy
- Cancer therapeutics and mechanisms
- Wound Healing and Treatments
- Chronic Kidney Disease and Diabetes
- Muscle Physiology and Disorders
- Adenosine and Purinergic Signaling
- Renal Diseases and Glomerulopathies
- DNA Repair Mechanisms
- RNA Interference and Gene Delivery
- Biomedical Research and Pathophysiology
- interferon and immune responses
- Calcium signaling and nucleotide metabolism
- Cell Adhesion Molecules Research
- Signaling Pathways in Disease
- Cellular Mechanics and Interactions
- Mitochondrial Function and Pathology
- Ion channel regulation and function
- Bioactive Compounds and Antitumor Agents
- Organ Transplantation Techniques and Outcomes
- Inflammasome and immune disorders
- High Altitude and Hypoxia
- Biochemical Acid Research Studies
The Ohio State University
2013-2023
Salem VA Medical Center
2020-2021
Carilion Roanoke Memorial Hospital
2021
Baylor College of Medicine
2017
Texas Children's Hospital
2017
The Ohio State University Wexner Medical Center
2013-2016
Rutgers, The State University of New Jersey
1996-2016
Lung Institute
2014-2016
Johnson University
1996-2015
Oklahoma State University Medical Center
2013
Recombinant MG53 translocates to sites of injury in the proximal tubule kidney and protects mice from acute induced by ischemia or drugs.
Following myocardial infarction (MI), degradation of extracellular matrix (ECM) by upregulated metalloproteinases (MMPs) especially MMP-2 decreases tissue mechanical properties, leading to cardiac function deterioration. Attenuation ECM at the early stage MI has potential preserve resulting in increase. Yet strategy for efficiently preventing remains be established. Current preclinical approaches have shown limited efficacy because low drug dosage allocated heart tissue, dose-limiting side...
Kidney fibrosis is associated with the progression of acute kidney injury to chronic disease. MG53, a cell membrane repair protein, has been shown protect against epithelial cells and injury. Here, we evaluated role MG53 in modulation aging mice unilateral ureteral obstruction (UUO) known model progressive fibrosis. Mice ablation developed more interstitial age than MG53-intact same age. Similarly, absence was exaggerated compared intact obstructed contralateral unobstructed or kidneys sham...
Induction of heme oxygenase (HO)-1 is a key defense mechanism against oxidative stress. Compared with tubules, glomeruli are refractory to HO-1 upregulation in response injury. This can be disadvantage as it may associated insufficient production cytoprotective heme-degradation metabolites. We, therefore, explored whether 1) targeted expression achieved without altering their physiological integrity and 2) this reduces proteinuria immune injury induced by an anti-glomerular basement membrane...
Overproduction of superoxide (O2*) occurs in glomerular disease and may overwhelm the capacity dismutase (SOD), thereby intensifying oxidant injury by O2* related radical species that disrupt capillary permeability barrier to protein. We examined efficacy SOD mimetic tempol preserving protein using 1) a rat model immune induced an antiglomerular basement membrane antibody (anti-GBM), 2) isolated glomeruli which was cytokine tumor necrosis factor-alpha (TNFalpha). To induce injury, rats...
Maintaining homeostatic Ca(2+) signaling is a fundamental physiological process in living cells. sparks are the elementary units of striated muscle fibers that appear as highly localized release events mediated by ryanodine receptor (RyR) channels on sarcoplasmic reticulum (SR) membrane. Proper assessment could provide information intracellular handling properties healthy and diseased muscles. Although commonly seen resting cardiomyocytes, they rarely observed skeletal fibers; thus there...
<h3></h3> Mesangial cell apoptosis has been proposed as a means of resolution glomerular hypercellularity in proliferative forms disease. We previously demonstrated that adenosine causes mesangial by stimulating the A<sub>3</sub>-type receptor. This is G protein-coupled receptor shown to activate kinases involved apoptotic signaling. In this work, we assessed changes phosphorylation mitogen-activated protein kinase extracellular signal-regulated (ERK)1/2 and levels specific pro-...
In glomerular immune injury, the inducible isoform of nitric oxide synthase (iNOS) becomes a major catalyst NO production. Although iNOS-catalyzed production is sustained and can be cytotoxic, iNOS inhibition exacerbates magnitude proteinuria that accompanies injury. To investigate putative mechanisms this effect, we assessed changes in permeability to albumin by using following two approaches: (i) an vivo rat model injury induced antibody against basement membrane (GBM), which urine...
The state of cellular chromatin in response to DNA damage has been examined by monitoring the change linking number circular episomes. COS cells transfected with an SV40-based vector were treated camptothecin (CPT), a eukaryotic topoisomerase I (TOPI) poison which induces TOP1-mediated damage. Within minutes, large increase (over 10 number) small fraction (5−15%) episomal was observed. A similar CPT-induced plasmid observed Saccharomyces cerevisae expressing human TOP1. In this case,...
The data presented pertain to a research article titled "Heme Oxygenase 1 Up-Regulates Glomerular Decay Accelerating Factor Expression and Minimizes Complement Deposition Injury" (Detsika et al., 2016). present work provides additional on induction immunolocalization of heme oxygenase (HO)-1 (an antioxidant enzyme) decay-accelerating factor (DAF) (a complement activation inhibitor) in isolated rat glomeruli glomerular epithelial cells (podocytes) response Iron Protoporphyrin IX (FePP, heme),...