A5101770133- Cell death mechanisms and regulation
- Retinoids in leukemia and cellular processes
- Ubiquitin and proteasome pathways
- Genomics, phytochemicals, and oxidative stress
- interferon and immune responses
- Mitochondrial Function and Pathology
- Nitric Oxide and Endothelin Effects
- Estrogen and related hormone effects
- Bioactive Compounds and Antitumor Agents
- Sulfur Compounds in Biology
- Eicosanoids and Hypertension Pharmacology
- Glutathione Transferases and Polymorphisms
- Curcumin's Biomedical Applications
- Peroxisome Proliferator-Activated Receptors
- Synthesis and biological activity
- MicroRNA in disease regulation
- Advanced Glycation End Products research
- Cancer-related Molecular Pathways
- Adipose Tissue and Metabolism
- Tannin, Tannase and Anticancer Activities
- DNA Repair Mechanisms
- Insect and Pesticide Research
- Antioxidant Activity and Oxidative Stress
- Pharmacological Effects and Assays
- RNA modifications and cancer
Mayo Clinic in Florida
2023
Zunyi Medical University
2016-2022
Soochow University
2017-2022
First Affiliated Hospital of Soochow University
2017-2022
Air Force Medical University
2008-2021
University of Minnesota Medical Center
2018-2020
Diabetes Australia
2016
University of Utah
2012-2016
Northeast Normal University
2010-2015
Yong In University
2012
Significance Smyd1 is a muscle-specific histone methyltransferase, and its role in the regulation of growth differentiation skeletal cardiac muscle well established. However, despite persistent expression postnatal cardiomyocytes, adult heart largely unknown. We show that regulates energy metabolism heart. Cardiac-specific ablation mouse resulted global downregulation mitochondrial proteins involved oxidative phosphorylation, concurrent with reduced respiration capacity. further demonstrate...
Obesity and insulin resistance are associated with oxidative stress (OS). The causal role of adipose OS in the pathogenesis these conditions is unknown. To address this issue, we generated mice an adipocyte-selective deletion manganese superoxide dismutase (MnSOD). When fed a high-fat diet (HFD), AdSod2 knockout (KO) exhibited less adiposity, reduced adipocyte hypertrophy, decreased circulating leptin. to diet-induced adiposity was result increased metabolic rate energy expenditure....
Although members of the hyaluronan (HA)‐CD44/HA‐mediated motility receptor (RHAMM) signaling pathway have been shown to be overexpressed in lung cancer, their role tumorigenesis is unclear. In present study, we first determined levels HA and its receptors CD44 RHAMM human non‐small cell cancer (NSCLC) cells stromal as well mouse tumors. Subsequently, examined HA‐CD44/RHAMM mediating proliferation survival NSCLC cross‐talk between normal fibroblasts (NHLFs)/lung cancer‐associated (LCAFs). The...
We investigated the in vitro effects of arsenic trioxide on cell growth, cycle regulation, and apoptosis As4.1 juxtaglomerular cells. Arsenic inhibited growth cells with an IC(50) approximately 5 microM. induced S phase arrest very efficiently stimulated cells, as evidenced by flow cytometric detection sub-G(1) DNA content, annexin V binding assay, 4'-6-diamidino-2-phenylindole staining. This apoptotic process was accompanied loss mitochondrial transmembrane potential (DeltaPsi(m)), a...
This study sought to elucidate the relationship between skeletal muscle mitochondrial dysfunction, oxidative stress, and insulin resistance in two mouse models with differential susceptibility diet-induced obesity. We examined time course of dysfunction obesity-prone C57B obesity-resistant FVB strains response high-fat feeding. After 5 wk, impaired insulin-mediated glucose uptake developed both absence any impairment proximal signaling. Impaired capacity preceded development resistant mice...
These studies investigate the role of uncoupling protein 3 (UCP3) in cardiac energy metabolism, O2 consumption (MVO2), efficiency (CE), and mitochondrial high fat (HF)–fed or leptin-deficient mice. UCP3KO wild-type (WT) mice were fed normal chow HF diets for 10 weeks. Substrate utilization rates, MVO2, CE, measured perfused working hearts saponin-permeabilized fibers, respectively. Similar analyses performed ob/ob lacking UCP3 (U3OB mice). increased protein. However, fatty acid (FA)...
The production of 20-hydroxyeicosatetraenoic acid (20-HETE) is increased during ischemia-reperfusion, and inhibition 20-HETE has been shown to reduce infarct size caused by ischemia. This study was aimed discover the molecular mechanism underlying action in cardiac myocytes. effect on L-type Ca 2+ currents ( I Ca,L ) examined rat isolated cardiomyocytes patch-clamp recording whole cell mode. Superfusion with (10–100 nM) resulted a concentration-dependent increase , this attenuated specific...
Background: It has been reported that 20-hydroxyeicosatetraenoic acid (20-HETE) aggravates myocardial ischemia/reperfusion (I/R) injury, but the exact mechanism of action is still unclear. Methods and Results: Experiments were performed in isolated rat hearts subjected to 35min ischemia followed by 40min reperfusion Langendorff preparations. Perfusion with HET0016, an inhibitor 20-HETE production, significantly improved I/R-induced reduction cardiac contractility, infarction, apoptosis. In...
Abstract Chronic obstructive pulmonary disease (COPD) is a significant risk factor for lung cancer. One potential mechanism through which COPD contributes to cancer development could be generation of an immunosuppressive microenvironment that allows tumor formation and progression. In this study, we compared the status immune cells checkpoint proteins in tumors induced by tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) or NNK + lipopolysaccharide (LPS), model...
Arsenic trioxide (ATO) affects many biological processes such as cell proliferation, apoptosis, differentiation and angiogenesis. L-buthionine sulfoximine (BSO) is an inhibitor of GSH synthesis. We tested whether ATO reduced the viability lung cancer A549 cells in vitro, investigated vitro effect combination BSO on relation to apoptosis cycle. caused a dose-dependant decrease with IC50 more than 50 μM. Low doses or (1~10 μM) alone did not induce death. However, combined treatment depleted...
Abstract Arsenic trioxide (ATO) can regulate many biological functions such as apoptosis and differentiation in various cells. We investigated an involvement of ROS H 2 O , GSH ATO‐treated Calu‐6 cell death. The levels intracellular were decreased cells at 72 h. However, the significantly increased. ATO reduced content. Many having depleted contents dead, evidenced by propidium iodine staining. activity CuZn‐SOD was strongly down‐regulated h while Mn‐SOD weakly up‐regulated. catalase ATO....
Arsenic trioxide (ATO) can regulate many biological functions such as apoptosis and differentiation. We evaluated the effects of ATO on various cell types cervical cancer HeLa cells, pulmonary adenocarcinoma Calu-6 A549 calf artery endothelial cells (CPAEC), human umbilical vein (HUVEC) fibroblast (HPF) in relation to growth, death reactive oxygen species (ROS) glutathione (GSH) levels. The growth was inhibited by with an IC50 approximately 15 microM at 24 h. not ATO. susceptibility CPAEC...
Arsenic trioxide (ATO) can affect many biological functions such as apoptosis and differentiation in various cells. We investigated the involvement of ROS GSH ATO-induced HeLa cell death using scavengers, especially N-acetylcysteine (NAC). ATO increased intracellular O2•- levels reduced content. The Tempol, Tiron Trimetazidine, did not significantly reduce or depletion ATO-treated Nor they induced by ATO. In contrast, treatment with NAC cells prevented apoptosis. Treatment exogenous SOD...
Cardiomyocyte apoptosis is involved in a variety of cardiac stresses, including ischemia-reperfusion injury, heart failure, and cardiomyopathy. Both Angiotensin II (Ang II) 20-hydroxyeicosatetraenoic acid (20-HETE) induce cardiomyocytes. Here, we examined the relationship between 20-HETE Ang cardiomyocyte apoptosis. Apoptosis was using flow cytometry primary cultured rat cardiomyocytes treated with control, II, plus HET0016 (a formation inhibitor). The results demonstrated that treatment or...