A5004628839- Mitochondrial Function and Pathology
- Metabolism and Genetic Disorders
- Organ Transplantation Techniques and Outcomes
- Eicosanoids and Hypertension Pharmacology
- Liver Disease Diagnosis and Treatment
- Calpain Protease Function and Regulation
- Sulfur Compounds in Biology
- Adipose Tissue and Metabolism
- Cardiac Ischemia and Reperfusion
- Spinal Cord Injury Research
- Renal and related cancers
- Acute Kidney Injury Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Peroxisome Proliferator-Activated Receptors
- Connexins and lens biology
- Ion Transport and Channel Regulation
- Drug-Induced Hepatotoxicity and Protection
- Cell death mechanisms and regulation
- Liver physiology and pathology
- Metabolomics and Mass Spectrometry Studies
- Liver Disease and Transplantation
- Pharmacogenetics and Drug Metabolism
- Nitric Oxide and Endothelin Effects
- Chemotherapy-induced organ toxicity mitigation
University of Arizona
2016-2025
Southern Arizona VA Health Care System
2017-2024
Arizona Science Center
2018-2024
Center for Innovation
2018-2024
University of Montana
2023
United States Department of Veterans Affairs
2014-2022
Veterans Health Administration
2022
Stanford University
2021
Medical University of South Carolina
2008-2017
Ralph H. Johnson VA Medical Center
2004-2016
The chemotherapeutic cisplatin causes renal dysfunction and proximal tubular cell (RPTC) apoptosis. goal of these studies was to examine the role p53, caspase 3, 8, 9, mitochondria in signaling cisplatin-induced Cisplatin (50 μM) produced time-dependent apoptosis RPTCs, causing shrinkage, a 50-fold increase 3 activity, 4-fold phosphatidylserine externalization, 5- 15-fold increases chromatin condensation DNA hypoploidy, respectively. Mitochondrial membrane potential ATP levels did not change...
This unit presents methods used to assess cell death in mammalian cells. The is divided into five sections: (1) a brief overview of cytotoxicity and pathways death, (2) an improved method measure using lactate dehydrogenase (LDH) release as marker membrane integrity, (3) flow cytometry that simultaneously measures two types oncosis apoptosis, (4) use nuclear morphology apoptosis oncosis, (5) discussion the assays determine mechanisms death.
Mitochondrial damage is often both the cause and outcome of cell injury resulting from a variety toxic insults, hypoxia, or trauma. Increasing mitochondrial biogenesis after renal proximal tubular (RPTC) accelerated recovery cellular functions (<i>Biochem Biophys Res Commun</i><b>355:</b>734–739, 2007). However, few pharmacological agents are known to increase biogenesis. We report that daidzein, genistein, biochanin A, formononetin, 3-(2′,4′-dichlorophenyl)-7-hydroxy-4<i>H</i>-chromen-4-one...
Rationale: Cigarette smoke (CS) inhalation triggers oxidative stress and inflammation, leading to accelerated lung aging, apoptosis, emphysema, as well systemic pathologies. Metformin is beneficial for protecting against aging-related diseases. Objectives: We sought investigate whether metformin may ameliorate CS-induced pathologies of emphysematous chronic obstructive pulmonary disease (COPD). Methods: Mice were exposed chronically CS fed metformin-enriched chow the second half exposure....
The goal of this study was to evaluate changes in metabolic homeostasis during the first 12 weeks recovery a distal middle cerebral artery occlusion mouse model stroke. To achieve goal, we compared brain metabolomes ipsilateral and contralateral hemispheres from aged male mice up after stroke that age-matched naïve sham mice. There were 707 biochemicals detected each sample by liquid chromatography-mass spectroscopy (LC-MS). Mitochondrial fatty acid β-oxidation, indicated acyl carnitine...
The characteristics of spiperone inhibition [3H]5-hydroxytryptamine [(3H]5-HT; [3H]serotonin) binding were examined in dorsal (DH) and ventral (VH) hippocampus, corpus striatum (CS) or caudate nucleus (CN), frontal cortex (FC) the rabbit, guinea pig, cat. Some properties [3H]5-HT these species similar to previously found rat. Spiperone was significantly more potent DH, VH, FC than CS CN. It produced shallow biphasic curves, resulting Hill slopes less 1.0. Nonlinear regression analysis data...
Abstract Methods for assessing mammalian cell death are presented in this unit. The unit is divided into six sections: (1) a brief overview of cytotoxicity and pathways death, (2) method to measure using lactate dehydrogenase (LDH) release as marker membrane integrity, (3) flow cytometry that simultaneously measures two types necrosis, apoptosis, (4) use fluorescence microscopy nuclear morphology assess apoptosis (5) the multi‐well plates high‐content analysis imaging systems morphology, (6)...
Acute kidney injury (AKI) is a common and potentially life-threatening complication after ischemia/reperfusion exposure to nephrotoxic agents. In this study, we examined the efficacy mechanism(s) of suramin in promoting recovery from glycerol-induced AKI, model rhabdomyolysis-induced AKI. After intramuscular glycerol injection (10 ml 50% per kilogram) into male Sprague-Dawley rats, serum creatinine maximally increased at 24 72 h then decreased 120 h. Creatinine clearance (CrCl) 75% Suramin...
Mitochondrial dysfunction is a common mediator of disease and organ injury. Although recent studies show that inducing mitochondrial biogenesis (MB) stimulates cell repair regeneration, only limited number chemicals are known to induce MB. To examine the impact β-adrenoceptor (β-AR) signaling pathway on MB, primary renal proximal tubule cells (RPTC) adult feline cardiomyocytes were exposed for 24 h multiple β-AR agonists: isoproterenol (nonselective agonist),...
Recent studies demonstrate that mitochondrial dysfunction is a mediator of acute kidney injury (AKI). Consequently, restoration function after AKI may be key to the recovery renal function. Mitochondrial can restored through generation new, functional mitochondria in process called biogenesis (MB). Despite its potential therapeutic significance, very few pharmacological agents have been identified induce MB. To examine efficacy phosphodiesterase (PDE) inhibitors (PDE3: cAMP and cGMP...
A goal of the Tox21 program is to transit toxicity testing from traditional in vivo models vitro assays that assess how chemicals affect cellular responses and pathways. critical contribution NIH Chemical Genomics center (NCGC) implementation a quantitative high throughput screening (qHTS) approach, using cell- biochemical-based generate toxicological profiles for thousands environmental compounds. Here, we evaluated effect chemical compounds on mitochondrial membrane potential HepG2 cells...
Our previous studies showed that an extract from Camellia sinenesis (green tea), which contains several polyphenols, attenuates nephrotoxicity caused by cyclosporine A (CsA). Since polyphenols are stimulators of mitochondrial biogenesis (MB), this study investigated whether stimulation MB plays a role in green tea polyphenol protection against CsA renal toxicity. Rats were fed powdered diet containing polyphenolic (0.1%) starting 3 days prior to treatment (25 mg/kg, i.g. daily for weeks)....
Many acute and chronic conditions, such as kidney injury, disease, heart failure, liver involve mitochondrial dysfunction. Although we have provided evidence that drug-induced stimulation of biogenesis (MB) accelerates cellular repair, leading to recovery organ function, only a limited number chemicals been identified induce MB. The goal this study was assess the role 5-hydroxytryptamine 1F (5-HT<sub>1F</sub>) receptor in Immunoblot quantitative polymerase chain reaction analyses revealed...