Carol R Gardner

Summary

Affiliation: Rutgers University
Country: USA

Publications

  1. pmc Potential role of caveolin-1 in acetaminophen-induced hepatotoxicity
    Carol R Gardner
    Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854, USA
    Toxicol Appl Pharmacol 245:36-46. 2010
  2. ncbi request reprint Exaggerated hepatotoxicity of acetaminophen in mice lacking tumor necrosis factor receptor-1. Potential role of inflammatory mediators
    Carol R Gardner
    Environmental and Occupational Health Sciences Institute, Rutgers University and University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway, NJ 08854 8020, USA
    Toxicol Appl Pharmacol 192:119-30. 2003
  3. ncbi request reprint Role of tumor necrosis factor receptor 1 (p55) in hepatocyte proliferation during acetaminophen-induced toxicity in mice
    Hawjyh Chiu
    Environmental and Occupational Health Sciences Institute, Rutgers University and University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway, NJ 08854 8020, USA
    Toxicol Appl Pharmacol 193:218-27. 2003
  4. ncbi request reprint Superoxide dismutase-overexpressing mice are resistant to ozone-induced tissue injury and increases in nitric oxide and tumor necrosis factor-alpha
    Ladan Fakhrzadeh
    Environmental and Occupational Health Science Institute, Rutgers University, Piscataway, NJ, USA
    Am J Respir Cell Mol Biol 30:280-7. 2004
  5. ncbi request reprint Role of p55 tumor necrosis factor receptor 1 in acetaminophen-induced antioxidant defense
    Hawjyh Chiu
    Dept of Pharmacology and Toxicology, Rutgers Univ, 170 Frelinghuysen Rd, Piscataway, NJ 08854 8020, USA
    Am J Physiol Gastrointest Liver Physiol 285:G959-66. 2003
  6. pmc Classical and alternative activation of rat hepatic sinusoidal endothelial cells by inflammatory stimuli
    Yinglin Liu
    Department of Pharmacology and Toxicology, Rutgers University Ernest Mario School of Pharmacy, 160 Frelinghuysen Rd, Piscataway, NJ 08854, USA
    Exp Mol Pathol 94:160-7. 2013
  7. pmc Regulation of alternative macrophage activation in the liver following acetaminophen intoxication by stem cell-derived tyrosine kinase
    Carol R Gardner
    Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854, USA
    Toxicol Appl Pharmacol 262:139-48. 2012
  8. pmc Exacerbation of acetaminophen hepatotoxicity by the anthelmentic drug fenbendazole
    Carol R Gardner
    Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, New Jersey 08854, USA
    Toxicol Sci 125:607-12. 2012
  9. ncbi request reprint Reduced hepatotoxicity of acetaminophen in mice lacking inducible nitric oxide synthase: potential role of tumor necrosis factor-alpha and interleukin-10
    Carol R Gardner
    Environmental and Occupational Health Sciences Institute, Rutgers University, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway 08854, USA
    Toxicol Appl Pharmacol 184:27-36. 2002
  10. pmc Macrophages and tissue injury: agents of defense or destruction?
    Debra L Laskin
    Department of Pharmacology and Toxicology, Rutgers University, Piscataway, New Jersey 08854, USA
    Annu Rev Pharmacol Toxicol 51:267-88. 2011

Collaborators

Detail Information

Publications14

  1. pmc Potential role of caveolin-1 in acetaminophen-induced hepatotoxicity
    Carol R Gardner
    Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854, USA
    Toxicol Appl Pharmacol 245:36-46. 2010
    ..Taken together, these data demonstrate that Cav-1 plays a role in promoting inflammation and toxicity during the pathogenesis of acetaminophen-induced injury...
  2. ncbi request reprint Exaggerated hepatotoxicity of acetaminophen in mice lacking tumor necrosis factor receptor-1. Potential role of inflammatory mediators
    Carol R Gardner
    Environmental and Occupational Health Sciences Institute, Rutgers University and University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway, NJ 08854 8020, USA
    Toxicol Appl Pharmacol 192:119-30. 2003
    ..In contrast, increases in IL-10 were more rapid and more pronounced. These data demonstrate that signaling through TNFR1 is important in inflammatory mediator production and toxicity induced by acetaminophen...
  3. ncbi request reprint Role of tumor necrosis factor receptor 1 (p55) in hepatocyte proliferation during acetaminophen-induced toxicity in mice
    Hawjyh Chiu
    Environmental and Occupational Health Sciences Institute, Rutgers University and University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway, NJ 08854 8020, USA
    Toxicol Appl Pharmacol 193:218-27. 2003
    ..Delayed cytokine signaling may account for reduced hepatocyte proliferation and contribute to exaggerated acetaminophen-induced hepatotoxicity in TNFR1-/- mice...
  4. ncbi request reprint Superoxide dismutase-overexpressing mice are resistant to ozone-induced tissue injury and increases in nitric oxide and tumor necrosis factor-alpha
    Ladan Fakhrzadeh
    Environmental and Occupational Health Science Institute, Rutgers University, Piscataway, NJ, USA
    Am J Respir Cell Mol Biol 30:280-7. 2004
    ..This response was significantly reduced in SOD+/+ mice. These data demonstrate that antioxidant enzymes play a critical role in ozone-induced tissue injury and in inflammatory mediator production...
  5. ncbi request reprint Role of p55 tumor necrosis factor receptor 1 in acetaminophen-induced antioxidant defense
    Hawjyh Chiu
    Dept of Pharmacology and Toxicology, Rutgers Univ, 170 Frelinghuysen Rd, Piscataway, NJ 08854 8020, USA
    Am J Physiol Gastrointest Liver Physiol 285:G959-66. 2003
    ..Reduced generation of antioxidants may contribute to the increased sensitivity of TNFR1-/- mice to acetaminophen...
  6. pmc Classical and alternative activation of rat hepatic sinusoidal endothelial cells by inflammatory stimuli
    Yinglin Liu
    Department of Pharmacology and Toxicology, Rutgers University Ernest Mario School of Pharmacy, 160 Frelinghuysen Rd, Piscataway, NJ 08854, USA
    Exp Mol Pathol 94:160-7. 2013
    ..The capacity of HSEC to respond to phenotypic activators may represent an important mechanism by which they participate in inflammatory responses associated with hepatotoxicity...
  7. pmc Regulation of alternative macrophage activation in the liver following acetaminophen intoxication by stem cell-derived tyrosine kinase
    Carol R Gardner
    Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854, USA
    Toxicol Appl Pharmacol 262:139-48. 2012
    ..These data demonstrate that STK plays a role in regulating macrophage recruitment and activation in the liver following acetaminophen administration, and in hepatotoxicity...
  8. pmc Exacerbation of acetaminophen hepatotoxicity by the anthelmentic drug fenbendazole
    Carol R Gardner
    Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, New Jersey 08854, USA
    Toxicol Sci 125:607-12. 2012
    ..These findings are novel and suggest a potential drug-drug interaction that should be considered in experimental protocols evaluating mechanisms of hepatotoxicity in rodent colonies treated with fenbendazole...
  9. ncbi request reprint Reduced hepatotoxicity of acetaminophen in mice lacking inducible nitric oxide synthase: potential role of tumor necrosis factor-alpha and interleukin-10
    Carol R Gardner
    Environmental and Occupational Health Sciences Institute, Rutgers University, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway 08854, USA
    Toxicol Appl Pharmacol 184:27-36. 2002
    ..Moreover, some of its effects may be mediated by altering production of pro- and antiinflammatory cytokines and proteins important in tissue repair...
  10. pmc Macrophages and tissue injury: agents of defense or destruction?
    Debra L Laskin
    Department of Pharmacology and Toxicology, Rutgers University, Piscataway, New Jersey 08854, USA
    Annu Rev Pharmacol Toxicol 51:267-88. 2011
    ....
  11. pmc Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity
    Srijata Sarkar
    Department of Environmental and Occupational Health, University of Medicine and Dentistry of New Jersey School of Public Health, Piscataway, NJ 08854, USA
    J Immunol 188:2778-93. 2012
    ..tuberculosis infection, inducing a hyporesponsive cellular state. Therefore, DEP alters crucial components of antimycobacterial host immune responses, providing a possible mechanism by which air pollutants alter antimicrobial immunity...
  12. ncbi request reprint Induction of cyclooxygenase-2 by heat shock protein 60 in macrophages and endothelial cells
    Blase Billack
    Department of Pharmacology and Toxicology, Rutgers University, Piscataway, NJ 08854, USA
    Am J Physiol Cell Physiol 283:C1267-77. 2002
    ..These data indicate that both ERK1/2 kinase and p38 kinase play a role in regulating HSP60-induced expression of COX-2...
  13. ncbi request reprint Nasal effects of a mixture of volatile organic compounds and their ozone oxidation products
    Robert J Laumbach
    Environmental and Occupational Health Sciences Institute, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
    J Occup Environ Med 47:1182-9. 2005
    ....
  14. ncbi request reprint Acute endotoxemia prolongs the survival of rat lung neutrophils in response to 12-O-tetradecanoyl-phorbol 13-acetate
    Vasanthi R Sunil
    Department of Pharmacology and Toxicology, Rutgers University, Piscataway, New Jersey 08854, USA
    J Cell Physiol 190:382-9. 2002
    ..Moreover, this response was independent of TPA. These data suggest that NF-kappaB plays a role in TPA-induced signaling leading to prolonged survival of adherent vascular neutrophils in the lung during acute endotoxemia...