Michael Rosenfeld

Summary

Affiliation: University of Washington
Country: USA

Publications

  1. pmc Inflammation and atherosclerosis: direct versus indirect mechanisms
    Michael E Rosenfeld
    Department of Pathology, University of Washington, USA
    Curr Opin Pharmacol 13:154-60. 2013
  2. ncbi request reprint An overview of the evolution of the atherosclerotic plaque: from fatty streak to plaque rupture and thrombosis
    M E Rosenfeld
    Department of Pathobiology, University of Washington, Seattle 98195, USA
    Z Kardiol 89:2-6. 2000
  3. ncbi request reprint Estrogen inhibits the initiation of fatty streaks throughout the vasculature but does not inhibit intra-plaque hemorrhage and the progression of established lesions in apolipoprotein E deficient mice
    Michael E Rosenfeld
    Department of Pathology, University of Washington, Seattle, WA 98195, USA
    Atherosclerosis 164:251-9. 2002
  4. pmc Progression and disruption of advanced atherosclerotic plaques in murine models
    Michael E Rosenfeld
    Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98109, USA
    Curr Drug Targets 9:210-6. 2008
  5. doi request reprint Pathogens and atherosclerosis: update on the potential contribution of multiple infectious organisms to the pathogenesis of atherosclerosis
    M E Rosenfeld
    Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98109 4714, USA
    Thromb Haemost 106:858-67. 2011
  6. ncbi request reprint Advanced atherosclerotic lesions in the innominate artery of the ApoE knockout mouse
    M E Rosenfeld
    Department of Pathology, University of Washington, Seattle 98195, USA
    Arterioscler Thromb Vasc Biol 20:2587-92. 2000
  7. ncbi request reprint Chlamydia, inflammation, and atherogenesis
    M E Rosenfeld
    Department of Pathobiology and Interdisciplinary Graduate Program in Nutritional Sciences, University of Washington, Seattle, WA 98195
    J Infect Dis 181:S492-7. 2000
  8. ncbi request reprint Chlamydia pneumoniae infection accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice
    T C Moazed
    Immunobiology Department, Immunex Crporation, Seattle, WA 98101 2936, USA
    J Infect Dis 180:238-41. 1999
  9. ncbi request reprint Chlamydia pneumoniae infection accelerates hyperlipidemia induced atherosclerotic lesion development in C57BL/6J mice
    E Blessing
    Department of Pathobiology, University of Washington, Box 357238, Seattle, WA 98195, USA
    Atherosclerosis 158:13-7. 2001
  10. ncbi request reprint Initiation of hyperinsulinemia and hyperleptinemia is diet dependent in C57BL/6 mice
    R A Harte
    Department of Pathobiology and Nutritional Sciences Interdisciplinary Program, University of Washington, Seattle, USA
    Horm Metab Res 31:570-5. 1999

Research Grants

  1. C. Pneumoniae and atherosclerotic plaque destabilization
    Michael Rosenfeld; Fiscal Year: 2007
  2. Glutathione, macrophages and unstable atherosclerosis
    Michael Rosenfeld; Fiscal Year: 2007
  3. Diesel Exhaust and Atherosclerotic Plaque Stability
    Michael Rosenfeld; Fiscal Year: 2007
  4. 2007 Atherosclerosis Gordon Research Conference
    Michael Rosenfeld; Fiscal Year: 2007
  5. HOMOCYSTEINE, INFLAMMATION, AND ATHEROGENESIS
    Michael Rosenfeld; Fiscal Year: 2001
  6. C. Pneumoniae and atherosclerotic plaque destabilization
    Michael Rosenfeld; Fiscal Year: 2004
  7. C. Pneumoniae and atherosclerotic plaque destabilization
    Michael E Rosenfeld; Fiscal Year: 2010

Collaborators

Detail Information

Publications45

  1. pmc Inflammation and atherosclerosis: direct versus indirect mechanisms
    Michael E Rosenfeld
    Department of Pathology, University of Washington, USA
    Curr Opin Pharmacol 13:154-60. 2013
    ....
  2. ncbi request reprint An overview of the evolution of the atherosclerotic plaque: from fatty streak to plaque rupture and thrombosis
    M E Rosenfeld
    Department of Pathobiology, University of Washington, Seattle 98195, USA
    Z Kardiol 89:2-6. 2000
    ....
  3. ncbi request reprint Estrogen inhibits the initiation of fatty streaks throughout the vasculature but does not inhibit intra-plaque hemorrhage and the progression of established lesions in apolipoprotein E deficient mice
    Michael E Rosenfeld
    Department of Pathology, University of Washington, Seattle, WA 98195, USA
    Atherosclerosis 164:251-9. 2002
    ..These data suggest that estrogen inhibits the initiation of the fatty streak but does not alter the progression of established lesions through stages of instability and healing...
  4. pmc Progression and disruption of advanced atherosclerotic plaques in murine models
    Michael E Rosenfeld
    Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98109, USA
    Curr Drug Targets 9:210-6. 2008
    ..The advanced lesions in the innominate arteries of the apo E-/- mice may however be adequate models for studying vascular fibrosis and calcification...
  5. doi request reprint Pathogens and atherosclerosis: update on the potential contribution of multiple infectious organisms to the pathogenesis of atherosclerosis
    M E Rosenfeld
    Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98109 4714, USA
    Thromb Haemost 106:858-67. 2011
    ..We also discuss the failure of antibiotic trials and the question of persistent infection...
  6. ncbi request reprint Advanced atherosclerotic lesions in the innominate artery of the ApoE knockout mouse
    M E Rosenfeld
    Department of Pathology, University of Washington, Seattle 98195, USA
    Arterioscler Thromb Vasc Biol 20:2587-92. 2000
    ..The processes underlying these changes in the innominate artery of older apoE(-/-) mice could well be a model for the critical processes leading to the breakdown and healing of the human atherosclerotic plaque...
  7. ncbi request reprint Chlamydia, inflammation, and atherogenesis
    M E Rosenfeld
    Department of Pathobiology and Interdisciplinary Graduate Program in Nutritional Sciences, University of Washington, Seattle, WA 98195
    J Infect Dis 181:S492-7. 2000
    ..7 cells with modified forms of low-density lipoprotein increases the resistance of the cells to C. pneumoniae infection and also increases the susceptibility to the combined toxic effects of modified lipids and C. pneumoniae infection...
  8. ncbi request reprint Chlamydia pneumoniae infection accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice
    T C Moazed
    Immunobiology Department, Immunex Crporation, Seattle, WA 98101 2936, USA
    J Infect Dis 180:238-41. 1999
    ..There were no differences in total plasma cholesterol levels between groups. This study demonstrates that C. pneumoniae infection accelerates the progression of atherosclerosis in the aortic arch of apoE-deficient mice...
  9. ncbi request reprint Chlamydia pneumoniae infection accelerates hyperlipidemia induced atherosclerotic lesion development in C57BL/6J mice
    E Blessing
    Department of Pathobiology, University of Washington, Box 357238, Seattle, WA 98195, USA
    Atherosclerosis 158:13-7. 2001
    ..02). This study shows that chronic C. pneumoniae infection accelerates atherosclerotic lesion development in diet induced hypercholesterolemic mice, indicating that C. pneumoniae is a co-risk factor of hyperlipidemia in atherogenesis...
  10. ncbi request reprint Initiation of hyperinsulinemia and hyperleptinemia is diet dependent in C57BL/6 mice
    R A Harte
    Department of Pathobiology and Nutritional Sciences Interdisciplinary Program, University of Washington, Seattle, USA
    Horm Metab Res 31:570-5. 1999
    ..Because leptin levels were most reflective of changes in insulin, our data support a role for insulin in determining plasma leptin levels in mice...
  11. ncbi request reprint A 6 week course of azithromycin treatment has no beneficial effect on atherosclerotic lesion development in apolipoprotein E-deficient mice chronically infected with Chlamydia pneumoniae
    E Blessing
    Department of Pathobiology, University of Washington, Seattle, WA 98195, USA
    J Antimicrob Chemother 55:1037-40. 2005
    ..To evaluate whether antimicrobial chemotherapy prevents acceleration of atherosclerotic lesion development induced by infection with Chlamydia pneumoniae...
  12. ncbi request reprint Development of a lipoprotein based molecular imaging MR contrast agent for the noninvasive detection of early atherosclerotic disease
    L M Mitsumori
    Department of Radiology and Pathobiology, University of Washington, Seattle, WA, USA
    Int J Cardiovasc Imaging 20:561-7. 2004
    ....
  13. ncbi request reprint Low level expression of hormone-sensitive lipase in arterial macrophage-derived foam cells: potential explanation for low rates of cholesteryl ester hydrolysis
    R A Harte
    Department of Pathobiology and Interdisciplinary Program in Nutritional Sciences, University of Washington, Seattle, WA 98195, USA
    Atherosclerosis 149:343-50. 2000
    ..Thus, low level expression of HSL may partially account for the reduced NCEH activity observed in arterial foam cells isolated from atherosclerosis-susceptible species...
  14. pmc Prevention of hepatic apoptosis and embryonic lethality in RelA/TNFR-1 double knockout mice
    M E Rosenfeld
    Department of Pathology, University of Washington, Seattle, Washington 98195, USA
    Am J Pathol 156:997-1007. 2000
    ..However, the absence of both TNFR-1 signaling and RelA activity in newborn mice makes these animals susceptible to endogenous hepatic infection...
  15. pmc Expression of suppressors of cytokine signaling during liver regeneration
    J S Campbell
    University of Washington, Department of Pathology, Seattle, Washington 98195, USA
    J Clin Invest 107:1285-92. 2001
    ..Together, these results suggest that SOCS-3 may be a key component in downregulating STAT-3 signaling after PH and that SOCS-3 mRNA levels in the regenerating liver are regulated by IL-6...
  16. pmc Depletion of resident alveolar macrophages does not prevent Fas-mediated lung injury in mice
    R A Bem
    Research Service of the Veterans Affairs Puget Sound Health Care System, University of Washington, Seattle, Washington, USA
    Am J Physiol Lung Cell Mol Physiol 295:L314-25. 2008
    ..These results suggest that the lung inflammatory response to Fas activation is not primarily dependent on resident alveolar macrophages and may instead depend on cytokine release by alveolar epithelial cells...
  17. ncbi request reprint Plaque rupture in humans and mice
    Stephen M Schwartz
    Department of Pathology, 815 Mercer Street, Room 421, University of Washington, Seattle, WA 98109 4714, USA
    Arterioscler Thromb Vasc Biol 27:705-13. 2007
    ..The relevance of such well-defined, objective, descriptive observations in the mouse can be tested for relevance against data from human pathology...
  18. ncbi request reprint Melagatran reduces advanced atherosclerotic lesion size and may promote plaque stability in apolipoprotein E-deficient mice
    Florian Bea
    Medizinische Klinik III, Universitat Heidelberg, 69120 Heidelberg, Germany
    Arterioscler Thromb Vasc Biol 26:2787-92. 2006
    ..We assessed the hypothesis that melagatran, a direct thrombin inhibitor, attenuates plaque progression and promotes stability of advanced atherosclerotic lesions...
  19. pmc Chlamydia pneumoniae infection increases adherence of mouse macrophages to mouse endothelial cells in vitro and to aortas ex vivo
    Naohisa Takaoka
    Department of Pathobiology, University of Washington, Seattle, WA 98195, USA
    Infect Immun 76:510-4. 2008
    ..pneumoniae promotes the adherence of mononuclear phagocytes to the endothelium at the site of atherosclerotic lesion formation to promote the progression of atherosclerosis...
  20. ncbi request reprint Osteoprotegerin inactivation accelerates advanced atherosclerotic lesion progression and calcification in older ApoE-/- mice
    Brian J Bennett
    Department of Pathobiology, University of Washington, Seattle, WA 98195, USA
    Arterioscler Thromb Vasc Biol 26:2117-24. 2006
    ..The current study was designed to assess whether OPG plays a role in the progression and calcification of advanced atherosclerotic lesions in apoE(-/-) mice...
  21. ncbi request reprint Atherosclerotic lesions in the common coronary arteries of ApoE knockout mice
    Weicheng Hu
    Shandong Medical University, 44 Wenhuaxi Road, Jinan, Shandong 250012, PR China
    Cardiovasc Pathol 14:120-5. 2005
    ..The present study describes the distribution of atherosclerotic lesions in the coronary arteries of chow-fed 60-week-old male ApoE(-/-), 17-beta-estradiol-treated ApoE(-/-), and wild-type mice...
  22. ncbi request reprint Simvastatin inhibits expression of tissue factor in advanced atherosclerotic lesions of apolipoprotein E deficient mice independently of lipid lowering: potential role of simvastatin-mediated inhibition of Egr-1 expression and activation
    Florian Bea
    Department of Pathobiology, Box 353410, University of Washington, Seattle, WA 98195, USA
    Atherosclerosis 167:187-94. 2003
    ....
  23. ncbi request reprint Calcification of advanced atherosclerotic lesions in the innominate arteries of ApoE-deficient mice: potential role of chondrocyte-like cells
    Marcello Rattazzi
    Department of Pathobiology, University of Washington, Seattle, WA 98195, USA
    Arterioscler Thromb Vasc Biol 25:1420-5. 2005
    ..The time course, cell types, and mechanism(s) associated with calcification were investigated...
  24. ncbi request reprint Long-term administration of 3-deazaadenosine does not alter progression of advanced atherosclerotic lesions in apolipoprotein E-deficient mice
    Michael R Preusch
    Department of Internal Medicine III, University of Heidelberg, Germany
    J Cardiovasc Pharmacol 50:206-12. 2007
    ....
  25. pmc Tumor necrosis factor alpha plays a role in the acceleration of atherosclerosis by Chlamydia pneumoniae in mice
    Lee Ann Campbell
    Department of Pathobiology, Box 357238, University of Washington, Seattle, WA 98195, USA
    Infect Immun 73:3164-5. 2005
    ..No acceleration of atherosclerotic lesion development was observed in infected mice compared to uninfected mice, indicating that TNF-alpha plays a role in the acceleration of atherosclerosis by C. pneumoniae...
  26. ncbi request reprint Foam cell formation inhibits growth of Chlamydia pneumoniae but does not attenuate Chlamydia pneumoniae-induced secretion of proinflammatory cytokines
    Erwin Blessing
    Department of Pathobiology, University of Washington, Seattle 98195, USA
    Circulation 105:1976-82. 2002
    ....
  27. ncbi request reprint Norgestimate and medroxyprogesterone acetate do not attenuate the atheroprotective effects of 17beta-estradiol in ovariectomized, apolipoprotein E-deficient mice
    Jennifer M Shultz
    Interdisciplinary Graduate Program in Nutritional Sciences, University of Washington, Seattle 98195, USA
    Fertil Steril 82:1133-9. 2004
    ..To determine whether progestins counteract the cardioprotective effects of estrogen...
  28. ncbi request reprint Lesion progression and plaque composition are not altered in older apoE-/- mice lacking tumor necrosis factor-alpha receptor p55
    Erwin Blessing
    Department of Pathobiology, University of Washington, P O Box 353410, Seattle, WA 98195, USA
    Atherosclerosis 176:227-32. 2004
    ..Inflammatory processes are an integral component of the initiation, progression, and destabilization of atherosclerotic lesions. Tumor necrosis factor-alpha (TNF-alpha) is considered a primary mediator of inflammatory processes...
  29. ncbi request reprint Simvastatin promotes atherosclerotic plaque stability in apoE-deficient mice independently of lipid lowering
    Florian Bea
    Department of Pathobiology, Interdisciplinary Graduate Program in Nutritional Sciences, University of Washington, Seattle 98195, USA
    Arterioscler Thromb Vasc Biol 22:1832-7. 2002
    ..This study sought to determine whether simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has stabilizing effects on vulnerable atherosclerotic plaques that are independent of their lipid-lowering capabilities...
  30. ncbi request reprint Animal models of spontaneous plaque rupture: the holy grail of experimental atherosclerosis research
    Michael E Rosenfeld
    Department of Pathobiology, University of Washington, Box 353410, Seattle 98195, USA
    Curr Atheroscler Rep 4:238-42. 2002
    ....
  31. ncbi request reprint Chronic inhibition of cyclooxygenase-2 does not alter plaque composition in a mouse model of advanced unstable atherosclerosis
    Florian Bea
    Department of Pathobiology and the Interdisciplinary Graduate Program in Nutritional Sciences, University of Washington, Seattle, WA 98195, USA
    Cardiovasc Res 60:198-204. 2003
    ..The current study was designed to investigate whether administration of a Cox-2 inhibitor to older apolipoprotein E deficient (apo E-/-) mice with established lesions alters the composition and increases the stability of the lesions...
  32. pmc Chlamydia pneumoniae and hyperlipidemia are co-risk factors for atherosclerosis: infection prior to induction of hyperlipidemia does not accelerate development of atherosclerotic lesions in C57BL/6J mice
    Erwin Blessing
    Department of Pathobiology, University of Washington, Seattle, Washington 98195, USA
    Infect Immun 70:5332-4. 2002
    ..pneumoniae did not accelerate lesion development in mice if a high-fat/high-cholesterol diet was started after infection, indicating that C. pneumoniae is a co-risk factor with hyperlipidemia for cardiovascular disease...
  33. ncbi request reprint Anti-atherosclerotic properties of telmisartan in advanced atherosclerotic lesions in apolipoprotein E deficient mice
    Erwin Blessing
    Medizinische Klinik III, Universitat Heidelberg, Heidelberg, Germany
    Atherosclerosis 199:295-303. 2008
    ....
  34. ncbi request reprint Arsenic exposure exacerbates atherosclerotic plaque formation and increases nitrotyrosine and leukotriene biosynthesis
    Melisa Bunderson
    Center for Environmental Health Sciences, University of Montana, Missoula, MT 59812 1552, USA
    Toxicol Appl Pharmacol 201:32-9. 2004
    ..In addition, amplified synthesis of reactive species such as peroxynitrite results in increased protein nitration in response to arsenic exposure. This finding is consistent with the pathology seen in human atherosclerotic plaques...
  35. ncbi request reprint Leukocyte recruitment into developing atherosclerotic lesions: the complex interaction between multiple molecules keeps getting more complex
    Michael E Rosenfeld
    Arterioscler Thromb Vasc Biol 22:361-3. 2002
  36. ncbi request reprint Putative murine models of plaque rupture
    Erling Falk
    Arterioscler Thromb Vasc Biol 27:969-72. 2007
  37. ncbi request reprint Induction of glutathione synthesis in macrophages by oxidized low-density lipoproteins is mediated by consensus antioxidant response elements
    Florian Bea
    Department of Pathobiology, University of Washington, Seattle, Wash 98195, USA
    Circ Res 92:386-93. 2003
    ..These data suggest that AREs play a direct role in mediating the induction of GSH synthesis by oxLDL and in protecting macrophages against oxidized lipid-induced oxidative stress...
  38. ncbi request reprint Neointimal cracks (plaque rupture?) and thrombosis in wrapped arteries without flow
    Erling Falk
    Arterioscler Thromb Vasc Biol 27:248-9; author reply 250-2. 2007
  39. ncbi request reprint Nitric oxide synthase plays a role in Chlamydia pneumoniae-induced atherosclerosis
    Brian B Chesebro
    Department of Pathobiology, University of Washington, P O Box 357238, Seattle, WA 98195, USA
    Cardiovasc Res 60:170-4. 2003
    ..Altered production of nitric oxide, a known bactericidal and anti-inflammatory agent, represents one possible mechanistic link. To examine this issue, a diet-induced, hyperlipidemic mouse model of early atherosclerosis was used...
  40. pmc Aggressive very low-density lipoprotein (VLDL) and LDL lowering by gene transfer of the VLDL receptor combined with a low-fat diet regimen induces regression and reduces macrophage content in advanced atherosclerotic lesions in LDL receptor-deficient mice
    Erin D MacDougall
    Dept of Pathology, 1959 NE Pacific St, University of Washington, Seattle, WA 98195 7470, USA
    Am J Pathol 168:2064-73. 2006
    ..These results show that aggressive VLDL/LDL lowering achieved by hepatic overexpression of VLDLR combined with a low-fat diet regimen induces regression of advanced plaques in the brachiocephalic artery of LDL receptor-deficient mice...
  41. ncbi request reprint Interleukin-10 suppresses tissue factor expression in lipopolysaccharide-stimulated macrophages via inhibition of Egr-1 and a serum response element/MEK-ERK1/2 pathway
    Motohiro Kamimura
    Department Internal Medicine III, University of Heidelberg, Heidelberg, Germany
    Circ Res 97:305-13. 2005
    ..Taken together, these results demonstrate a pathway for the IL-10 mediated inhibition of TF expression during inflammation and may explain the antiatherosclerotic effects of IL-10...
  42. pmc Effect of Chlamydia pneumoniae on cellular ATP content in mouse macrophages: role of Toll-like receptor 2
    Kambiz Yaraei
    Department of Pathobiology, Box 353410, University of Washington, Seattle, Washington 98195, USA
    Infect Immun 73:4323-6. 2005
    ..In contrast, no effect was observed in macrophages lacking expression of Toll-like receptor 4...
  43. pmc Chlamydia pneumoniae augments the oxidized low-density lipoprotein-induced death of mouse macrophages by a caspase-independent pathway
    Kambiz Yaraei
    Department of Pathobiology, Box 353410, University of Washington, Seattle, Washington 98195, USA
    Infect Immun 73:4315-22. 2005
    ..pneumoniae-induced death. These data suggest that C. pneumoniae kills cells by a caspase-independent pathway and that the process is potentially mediated by activation of TLR-2...
  44. ncbi request reprint Methionine-induced hyperhomocysteinemia promotes superoxide anion generation and NFkappaB activation in peritoneal macrophages of C57BL/6 mice
    Young Sun Song
    School of Food and Life Science and Food Science Institute, Inje University, Obang dong, Kimhae, Kyung nam, Korea
    J Med Food 7:229-34. 2004
    ..These results suggest that HHcy induced by methionine may intensify disturbances in peroxidation and inflammatory mediator activation in peritoneal macrophages, and is a possible mechanism of its atherogenic effects...
  45. ncbi request reprint Chlamydia pneumoniae infection and atherosclerosis: methodological considerations
    C C Kuo
    Circulation 105:E34. 2002

Research Grants22

  1. C. Pneumoniae and atherosclerotic plaque destabilization
    Michael Rosenfeld; Fiscal Year: 2007
    ..4. To determine whether exposure of young versus old mice to air pollution increases the susceptibility of the mice to C. pneumoniae infection and accelerates the development and progression of atherosclerosis. ..
  2. Glutathione, macrophages and unstable atherosclerosis
    Michael Rosenfeld; Fiscal Year: 2007
    ..abstract_text> ..
  3. Diesel Exhaust and Atherosclerotic Plaque Stability
    Michael Rosenfeld; Fiscal Year: 2007
    ....
  4. 2007 Atherosclerosis Gordon Research Conference
    Michael Rosenfeld; Fiscal Year: 2007
    ..The conference will provide a comprehensive overview of current research on atherosclerosis with a focus on the latest and most exciting developments in the field. ..
  5. HOMOCYSTEINE, INFLAMMATION, AND ATHEROGENESIS
    Michael Rosenfeld; Fiscal Year: 2001
    ..Under Aim 2, the investigator will determine the mechanism by which HC and lipid accumulation alter glutathione and NADH/NADPH metabolism, thereby activating macrophages in vitro. ..
  6. C. Pneumoniae and atherosclerotic plaque destabilization
    Michael Rosenfeld; Fiscal Year: 2004
    ..pneumoniae infection accelerates cell death and plaque destabilization and thus help explain why C. pneumoniae infection is associated with an increased risk of mortality from cardiovascular disease. ..
  7. C. Pneumoniae and atherosclerotic plaque destabilization
    Michael E Rosenfeld; Fiscal Year: 2010
    ..4. To determine whether exposure of young versus old mice to air pollution increases the susceptibility of the mice to C. pneumoniae infection and accelerates the development and progression of atherosclerosis. ..