Research Topics
Species | Q M ChenSummaryAffiliation: University of Arizona Country: USA Publications
Research Grants
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Publications
c-Fos phosphorylation induced by H2O2 prevents proteasomal degradation of c-Fos in cardiomyocytesJune Coronella-Wood
Department of Pharmacology, University of Arizona, College of Medicine, Tucson, Arizona 85724, USA
J Biol Chem 279:33567-74. 2004..PP2B independent dephosphorylation contributes to degradation of c-Fos protein during oxidative stress response of cardiomyocytes...- Involvement of oxidants and AP-1 in angiotensin II-activated NFAT3 transcription factorVictoria C Tu
Department of Pharmacology, Arizona Cancer Center, College of Medicine, University of Arizona, 1501 N Campbell Ave, Tucson, AZ 85724, USA
Am J Physiol Cell Physiol 292:C1248-55. 2007..Our data suggest that hypertrophy inducers ANG II and H(2)O(2) may activate NFAT3 in cardiomyocyte through an AP-1 transcription factor-dependent mechanism... - Apoptosis and heart failure: mechanisms and therapeutic implicationsQin M Chen
Department of Pharmacology, University of Arizona, College of Medicine, Tucson, Arizona 85724, USA
Am J Cardiovasc Drugs 2:43-57. 2002..These studies indicate the importance of inhibiting apoptosis in therapeutic interventions against heart failure... - Molecular mechanisms of cardiac hypertrophy induced by toxicantsQ M Chen
Department of Pharmacology, College of Medicine, University of Arizona, 1501 N Campbell Ave, Tucson, AZ 85724, USA
Cardiovasc Toxicol 1:267-83. 2001..Oxidants cause cardiomyocytes to enlarge in vitro. Recent developments in transgenic, genomic, and proteomic technologies will provide needed tools to reveal the mechanism of chronic cardiac toxicity at the cellular and molecular levels... - Down regulation of p53 with HPV E6 delays and modifies cell death in oxidant response of human diploid fibroblasts: an apoptosis-like cell death associated with mitosisQin M Chen
Department of Pharmacology, University of Arizona, College of Medicine, 1501 N Campbell Avenue, Tucson, Arizona, AZ 85724, USA
Oncogene 21:5313-24. 2002..Our data indicate that expression of HPV E6 causes a delay and morphological modification of cell death induced by oxidants. E6 cells die at mitosis, which can be inhibited by bcl-2 overexpression or caspase inhibition... - Corticosteroids inhibit cell death induced by doxorubicin in cardiomyocytes: induction of antiapoptosis, antioxidant, and detoxification genesQin M Chen
Department of Pharmacology, University of Arizona, 1501 N Campbell Avenue, Tucson, AZ 85724, USA
Mol Pharmacol 67:1861-73. 2005..Inhibiting the expression of bcl-xL reduced the cytoprotective effect of CT. Our data suggest that CT induces a cytoprotective effect on cardiomyocytes in association with reprogramming gene expression and induction of bcl-xL gene... - Apoptosis or senescence-like growth arrest: influence of cell-cycle position, p53, p21 and bax in H2O2 response of normal human fibroblastsQ M Chen
Department of Pharmacology, Skaggs Pharmaceutical Sciences Building, Room 130, University of Arizona, 1703 E Mabel Street, Tucson, AZ 85721, USA
Biochem J 347:543-51. 2000..Our data suggest that in contrast with growth-arrested cells, apoptotic cells show an S-phase cell cycle distribution, a higher degree of p53 elevation, an absence of p21 protein and increased solubility of bax protein... - Involvement of Rb family proteins, focal adhesion proteins and protein synthesis in senescent morphogenesis induced by hydrogen peroxideQ M Chen
Department of Pharmacology, University of Arizona, Skaggs Pharmaceutical Science Building, Tucson, AZ 85721, USA
J Cell Sci 113:4087-97. 2000..Our results suggest that senescent morphology likely develops by a program involving activated Rb family proteins, enhancement of actin stress fibers, redistribution of focal adhesion proteins and de novo protein synthesis... - Measurements of hydrogen peroxide induced premature senescence: senescence-associated beta-galactosidase and DNA synthesis index in human diploid fibroblasts with down-regulated p53 or RbQ M Chen
Department of Pharmacology and Toxicology, Skaggs Pharmaceutical Sciences Building, University of Arizona, Tucson, AZ 85721, USA
Biogerontology 1:335-9. 2000..The results indicate that the expression of SA beta-gal correlates with inability of DNA synthesis in the majority of wild type, E6, E7 or E6E7 expressing cells one week after H2O2 treatment... - Hydrogen peroxide dose dependent induction of cell death or hypertrophy in cardiomyocytesQ M Chen
Department of Pharmacology, University of Arizona, Skaggs Pharmaceutical Science Building, 1703 East Mabel Street, Tucson, Arizona, 85721, USA
Arch Biochem Biophys 373:242-8. 2000..The enlarged cells showed enhanced actin stress fibers and disrupted myofibrils. Our data indicate that while H(2)O(2) can cause cell death, the surviving cardiomyocytes undergo hypertrophy... - Replicative senescence and oxidant-induced premature senescence. Beyond the control of cell cycle checkpointsQ M Chen
Department of Pharmacology, University of Arizona, Tucson 85721, USA
Ann N Y Acad Sci 908:111-25. 2000.... - Proteomic identification of insulin-like growth factor-binding protein-6 induced by sublethal H2O2 stress from human diploid fibroblastsLifang Xie
Department of Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona 85724, USA
Mol Cell Proteomics 4:1273-83. 2005..These data suggest that IGFBP-6 may serve as a sensitive biomarker of cell degeneration or injury in vitro and in vivo... - Cystatin C increases in cardiac injury: a role in extracellular matrix protein modulationLifang Xie
Department of Pharmacology, College of Medicine, University of Arizona, 1501 N Campbell Ave, Tucson, AZ 85724, USA
Cardiovasc Res 87:628-35. 2010..Numerous lines of evidence suggest a role of oxidative stress in initiation and progression of heart failure. We identify novel pathways of oxidative stress in cardiomyocytes using proteomic technology... - Genomic and proteomic profiling of oxidative stress response in human diploid fibroblastsLifang Xie
Department of Pharmacology, College of Medicine, University of Arizona, 1501 N Campbell Ave, Tucson, AZ 85724, USA
Biogerontology 10:125-51. 2009..The low overlap suggests the importance of considering proteins instead of transcripts when investigating the gene expression profile altered by oxidative stress... - Arsenic alters vascular smooth muscle cell focal adhesion complexes leading to activation of FAK-src mediated pathwaysMichele D Pysher
Department of Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona 85724, USA
Toxicol Appl Pharmacol 231:135-41. 2008..Past studies have demonstrated that these pathways are involved in cellular survival, growth, proliferation, and migration in VSMCs... - Signals of oxidant-induced cardiomyocyte hypertrophy: key activation of p70 S6 kinase-1 and phosphoinositide 3-kinaseVictoria C Tu
Department of Pharmacology, College of Medicine, University of Arizona, Tucson, Arizona 85724, USA
J Pharmacol Exp Ther 300:1101-10. 2002..Our data suggest that oxidative stress induces activation of PI3K, which leads to p70S6K1 activation and enlargement of cell size... - Induction of antioxidant and detoxification response by oxidants in cardiomyocytes: evidence from gene expression profiling and activation of Nrf2 transcription factorSally E Purdom Dickinson
Interdisciplinary Graduate Program in Genetics and Genomics, University of Arizona, 1501 N Campbell Ave, Tucson, AZ 85724, USA
J Mol Cell Cardiol 42:159-76. 2007..Therefore, the cytoprotective effect of H(2)O(2) pretreatment is not reliant upon Nrf2 activation alone as measured by resistance against Dox-induced apoptosis... - Uncoupling the senescent phenotype from telomere shortening in hydrogen peroxide-treated fibroblastsQ M Chen
Department of Pharmacology, University of Arizona, Tucson, Arizona 85724 5050, USA
Exp Cell Res 265:294-303. 2001..The role of cell cycle checkpoints centered on p21 in premature senescence induced by H(2)O(2) is discussed here... - Epidermal growth factor receptor-dependent and -independent pathways in hydrogen peroxide-induced mitogen-activated protein kinase activation in cardiomyocytes and heart fibroblastsSally Purdom
Department of Pharmacology, College of Medicine, University of Arizona, 1501 North Campbell Ave, Tucson, AZ 85724, USA
J Pharmacol Exp Ther 312:1179-86. 2005..In contrast, these MMP failed to significantly inhibit the activation of JNKs, ERKs, or p38 in CMCs. These data suggest the complexity of the cell type-dependent signaling web initiated by oxidants in the heart... - P38 MAPK mediates COX-2 gene expression by corticosterone in cardiomyocytesHaipeng Sun
Department of Pharmacology, University of Arizona, 1501 N Campbell Ave, Tucson, AZ 85724, United States
Cell Signal 20:1952-9. 2008..Our data suggest that two parallel signaling pathways, glucocorticoid receptor and p38 MAPK, act in concert to regulate the expression of COX-2 gene in cardiomyocytes... - Novel mechanisms of sublethal oxidant toxicity: induction of premature senescence in human fibroblasts confers tumor promoter activityTarrah K Dilley
Department of Pharmacology, College of Medicine, University of Arizona, 1501 North Campbell Avenue, Tucson, AZ 85724, USA
Exp Cell Res 290:38-48. 2003.... - Translational control of nrf2 protein in activation of antioxidant response by oxidantsSally E Purdom Dickinson
Department of Pharmacology, University of Arizona College of Medicine, 1501 N Campbell Ave, Tucson, AZ 85724, USA
Mol Pharmacol 72:1074-81. 2007..The mechanism underlying such stress-induced de novo protein translation may involve multiple components of translational machinery... - Distinct roles of p42/p44(ERK) and p38 MAPK in oxidant-induced AP-1 activation and cardiomyocyte hypertrophyVictoria C Tu
Interdisciplinary Graduate Program in Pharmacology and Toxicology, College of Medicine, University of Arizona, Tucson, AZ 85724, USA
Cardiovasc Toxicol 3:119-33. 2003..These data suggest that while p42/p44(ERK) participates in gene expression associated with hypertrophy, p38 may regulate cell size increase by p70S6K1 activation... - Inhibitors of GSK-3 prevent corticosterone from inducing COX-1 expression in cardiomyocytesHaipeng Sun
Interdisciplinary Graduate Program of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, USA
Cardiovasc Toxicol 8:93-100. 2008..We conclude that GSK-3 inhibitors block CT from inducing COX-1 gene expression via a mechanism beyond GR and Sp3 transcription factor... - Corticosteroids induce cyclooxygenase 1 expression in cardiomyocytes: role of glucocorticoid receptor and Sp3 transcription factorHaipeng Sun
Interdisciplinary Graduate Program of Pharmacology and Toxicology, University of Arizona, 1501 North Campbell Avenue, Tucson, Arizona 85724, USA
Mol Endocrinol 22:2076-84. 2008..Our data suggest that activated GR interacts with Sp3 transcription factor in binding to COX-1 promoter to enhance COX-1 gene expression in cardiomyocytes... - Corticosteroids induce COX-2 expression in cardiomyocytes: role of glucocorticoid receptor and C/EBP-betaHaipeng Sun
Interdisciplinary Graduate Program of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona 85724, USA
Am J Physiol Cell Physiol 295:C915-22. 2008..Our data suggest that the interaction between GR and C/EBP-beta contributes to elevated COX-2 gene transcription by CT in cardiomyocytes... - p66(Shc): at the crossroad of oxidative stress and the genetics of agingSally Purdom
Interdisciplinary Graduate Program for Genetics and Genomics, University of Arizona, 1501 N. Campbell, Tucson, AZ 85724, USA
Trends Mol Med 9:206-10. 2003..This leads us to hypothesize that increased methylation of the p66(Shc) promoter might contribute to the absence of its expression and therefore extended longevity in particular individuals... - LY294002 inhibits glucocorticoid-induced COX-2 gene expression in cardiomyocytes through a phosphatidylinositol 3 kinase-independent mechanismHaipeng Sun
Interdisciplinary Graduate Program of Pharmacology and Toxicology, University of Arizona, Tucson, AZ 85724, USA
Toxicol Appl Pharmacol 232:25-32. 2008..CT was found to increase intracellular Ca(2+) concentration, which can be inhibited by LY29, TEA or nimodipine. These data suggest a possible role of calcium instead of PI3K in CT-induced COX-2 expression in cardiomyocytes... - Linking oxidative stress and genetics of aging with p66Shc signaling and forkhead transcription factorsSally Purdom
Interdisciplinary Graduate Program for Genetics and Genomics, University of Arizona, Tucson, AZ 85724, USA
Biogerontology 4:181-91. 2003..We present evidence arguing that decreasing oxidative stress or increasing resistance to oxidative damage as a result of genetic variation or p66Shc knockout is likely contributing to individual differences in longevity... - FP prostanoid receptor-mediated induction of the expression of early growth response factor-1 by activation of a Ras/Raf/mitogen-activated protein kinase signaling cascadeWei Xu
Department of Pharmacology and Toxicology, College of Pharmacy The University of Arizona, 1703 E Mabel St, Tucson, AZ 85721 0207, USA
Mol Pharmacol 73:111-8. 2008..This is the first report to show the regulation of EGR-1 expression after PGF(2alpha) activation of FP receptors and suggests that this could be an early event involved in wound healing and cardiac hypertrophy... - Partial proteasome inhibition in human fibroblasts triggers accelerated M1 senescence or M2 crisis depending on p53 and Rb statusNiki Chondrogianni
National Hellenic Research Foundation, Institute of Biological Research and Biotechnology, Athens, Greece
Aging Cell 7:717-32. 2008..These data reveal the continuous interplay between the integrity of proteasome function, senescence and cell survival...
Research Grants
- Translational Control of Oxidative Stress in Myocardial InfarctionQin M Chen; Fiscal Year: 2010..PUBLIC HEALTH RELEVANCE: This grant proposes to study the mechanism of Nrf2 protein translation in cardiomyocytes and in the myocardium following oxidative stress. ..
- Translational Control of Oxidative Stress in Myocardial InfarctionQin Chen; Fiscal Year: 2009..PUBLIC HEALTH RELEVANCE: This grant proposes to study the mechanism of Nrf2 protein translation in cardiomyocytes and in the myocardium following oxidative stress. ..
- Graduate Training Program in Toxicology and ToxicogenomicsQin Chen; Fiscal Year: 2007....
- Steroid As Cytoprotectants against Oxidative ToxicityQin Chen; Fiscal Year: 2007....
- MOLECULAR MECHANISMS OF OXIDANT TOXICITYQin Chen; Fiscal Year: 2004..We have a unique finding of premature senescence with oxidative stress and will combine in vitro and in vivo approaches to uncover the trigger of unwanted effects of aging. ..