View Item 

Show simple item record

Paradoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell disease
dc.contributor.authorWang, Huien_US
dc.contributor.authorLuo, Weien_US
dc.contributor.authorWang, Jintaoen_US
dc.contributor.authorGuo, Chiaoen_US
dc.contributor.authorWolffe, Stephanie L.en_US
dc.contributor.authorWang, Juliaen_US
dc.contributor.authorSun, Eddy B.en_US
dc.contributor.authorBradley, Kori N.en_US
dc.contributor.authorCampbell, Andrew D.en_US
dc.contributor.authorEitzman, Daniel T.en_US
dc.date.accessioned2013-06-18T18:32:09Z
dc.date.available2014-09-02T14:12:52Zen_US
dc.date.issued2013-07en_US
dc.identifier.citationWang, Hui; Luo, Wei; Wang, Jintao; Guo, Chiao; Wolffe, Stephanie L.; Wang, Julia; Sun, Eddy B.; Bradley, Kori N.; Campbell, Andrew D.; Eitzman, Daniel T. (2013). "Paradoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell disease." British Journal of Haematology 162(1): 120-129. <http://hdl.handle.net/2027.42/98139>en_US
dc.identifier.issn0007-1048en_US
dc.identifier.issn1365-2141en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/98139
dc.publisherWiley Periodicals, Inc.en_US
dc.subject.otherThrombosisen_US
dc.subject.otherAtherosclerosisen_US
dc.subject.otherBone Marrow Transplanten_US
dc.subject.otherHaem Oxygenaseen_US
dc.titleParadoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell diseaseen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelOncology and Hematologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.identifier.pmid23590132en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/98139/1/bjh12342.pdf
dc.identifier.doi10.1111/bjh.12342en_US
dc.identifier.sourceBritish Journal of Haematologyen_US
dc.identifier.citedreferenceMotterlini, R., Foresti, R., Vandegriff, K., Intaglietta, M. & Winslow, R.M. ( 1995 ) Oxidative‐stress response in vascular endothelial cells exposed to acellular hemoglobin solutions. American Journal of Physiology, 269, H648 – H655.en_US
dc.identifier.citedreferenceLivak, K.J. & Schmittgen, T.D. ( 2001 ) Analysis of relative gene expression data using real‐time quantitative PCR and the 2(‐Delta Delta C(T)) Method. Methods, 25, 402 – 408.en_US
dc.identifier.citedreferenceMaisel, A., Friedman, H., Flint, L., Koshy, M. & Prabhu, R. ( 1983 ) Continuous electrocardiographic monitoring in patients with sickle‐cell anemia during pain crisis. Clinical Cardiology, 6, 339 – 344.en_US
dc.identifier.citedreferenceManci, E.A., Culberson, D.E., Yang, Y.M., Gardner, T.M., Powell, R., Haynes, J. Jr, Shah, A.K. & Mankad, V.N. ( 2003 ) Causes of death in sickle cell disease: an autopsy study. British Journal of Haematology, 123, 359 – 365.en_US
dc.identifier.citedreferenceMansi, I.A. & Rosner, F. ( 2002 ) Myocardial infarction in sickle cell disease. Journal of the National Medical Association, 94, 448 – 452.en_US
dc.identifier.citedreferenceMartin, C.R., Johnson, C.S., Cobb, C., Tatter, D. & Haywood, L.J. ( 1996 ) Myocardial infarction in sickle cell disease. Journal of the National Medical Association, 88, 428 – 432.en_US
dc.identifier.citedreferenceMcCormick, W.F. ( 1988 ) Massive nonatherosclerotic myocardial infarction in sickle cell anemia. American Journal of Forensic Medicine and Pathology, 9, 151 – 154.en_US
dc.identifier.citedreferenceMehari, A., Gladwin, M.T., Tian, X., Machado, R.F. & Kato, G.J. ( 2012 ) Mortality in adults with sickle cell disease and pulmonary hypertension. JAMA, 307, 1254 – 1256.en_US
dc.identifier.citedreferenceMorris, C.R. ( 2011 ) Vascular risk assessment in patients with sickle cell disease. Haematologica, 96, 1 – 5.en_US
dc.identifier.citedreferenceMurphy, A.J., Akhtari, M., Tolani, S., Pagler, T., Bijl, N., Kuo, C.L., Wang, M., Sanson, M., Abramowicz, S., Welch, C., Bochem, A.E., Kuivenhoven, J.A., Yvan‐Charvet, L. & Tall, A.R. ( 2011 ) ApoE regulates hematopoietic stem cell proliferation, monocytosis, and monocyte accumulation in atherosclerotic lesions in mice. The Journal of Clinical Investigation, 121, 4138 – 4149.en_US
dc.identifier.citedreferenceNakashima, Y., Plump, A.S., Raines, E.W., Breslow, J.L. & Ross, R. ( 1994 ) ApoE‐deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree. Arteriosclerosis and Thrombosis, 14, 133 – 140.en_US
dc.identifier.citedreferenceOhman, M.K., Shen, Y., Obimba, C.I., Wright, A.P., Warnock, M., Lawrence, D.A. & Eitzman, D.T. ( 2008 ) Visceral adipose tissue inflammation accelerates atherosclerosis in apolipoprotein E‐deficient mice. Circulation, 117, 798 – 805.en_US
dc.identifier.citedreferenceOztas, Y., Durukan, I., Unal, S. & Ozgunes, N. ( 2012 ) Plasma protein oxidation is correlated positively with plasma iron levels and negatively with hemolysate zinc levels in sickle‐cell anemia patients. International Journal of Laboratory Hematology, 34, 129 – 135.en_US
dc.identifier.citedreferencePaine, A., Eiz‐Vesper, B., Blasczyk, R. & Immenschuh, S. ( 2010 ) Signaling to heme oxygenase‐1 and its anti‐inflammatory therapeutic potential. Biochemical Pharmacology, 80, 1895 – 1903.en_US
dc.identifier.citedreferencePlatt, O.S., Thorington, B.D., Brambilla, D.J., Milner, P.F., Rosse, W.F., Vichinsky, E. & Kinney, T.R. ( 1991 ) Pain in sickle cell disease. Rates and risk factors. New England Journal of Medicine, 325, 11 – 16.en_US
dc.identifier.citedreferencePlump, A.S., Smith, J.D., Hayek, T., Aalto‐Setala, K., Walsh, A., Verstuyft, J.G., Rubin, E.M. & Breslow, J.L. ( 1992 ) Severe hypercholesterolemia and atherosclerosis in apolipoprotein E‐deficient mice created by homologous recombination in ES cells. Cell, 71, 343 – 353.en_US
dc.identifier.citedreferenceRees, D.C., Williams, T.N. & Gladwin, M.T. ( 2010 ) Sickle‐cell disease. Lancet, 376, 2018 – 2031.en_US
dc.identifier.citedreferenceRoss, R. ( 1995 ) Cell biology of atherosclerosis. Annual Review of Physiology, 57, 791 – 804.en_US
dc.identifier.citedreferenceRothman, S.M., Fulling, K.H. & Nelson, J.S. ( 1986 ) Sickle cell anemia and central nervous system infarction: a neuropathological study. Annals Neurology, 20, 684 – 690.en_US
dc.identifier.citedreferenceRyan, T.M., Ciavatta, D.J. & Townes, T.M. ( 1997 ) Knockout‐transgenic mouse model of sickle cell disease. Science, 278, 873 – 876.en_US
dc.identifier.citedreferenceTongers, J., Fiedler, B., Konig, D., Kempf, T., Klein, G., Heineke, J., Kraft, T., Gambaryan, S., Lohmann, S.M., Drexler, H. & Wollert, K.C. ( 2004 ) Heme oxygenase‐1 inhibition of MAP kinases, calcineurin/NFAT signaling, and hypertrophy in cardiac myocytes. Cardiovascular Research, 63, 545 – 552.en_US
dc.identifier.citedreferenceViles‐Gonzalez, J.F., Fuster, V. & Badimon, J.J. ( 2004 ) Atherothrombosis: a widespread disease with unpredictable and life‐threatening consequences. European Heart Journal, 25, 1197 – 1207.en_US
dc.identifier.citedreferenceVillagra, J., Shiva, S., Hunter, L.A., Machado, R.F., Gladwin, M.T. & Kato, G.J. ( 2007 ) Platelet activation in patients with sickle disease, hemolysis‐associated pulmonary hypertension, and nitric oxide scavenging by cell‐free hemoglobin. Blood, 110, 2166 – 2172.en_US
dc.identifier.citedreferenceWang, Y., Huang, Z., Lu, H., Lin, H., Wang, Z., Chen, X., Ouyang, Q., Tang, M., Hao, P., Ni, J., Xu, D., Zhang, M., Zhang, Q., Lin, L. & Zhang, Y. ( 2012 ) Apolipoprotein E‐knockout mice show increased titers of serum anti‐nuclear and anti‐dsDNA antibodies. Biochemical and Biophysical Research Communications, 423, 805 – 812.en_US
dc.identifier.citedreferenceWestrick, R.J., Winn, M.E. & Eitzman, D.T. ( 2007 ) Murine models of vascular thrombosis (Eitzman series). Arteriosclerosis, Thrombosis, and Vascular Biology, 27, 2079 – 2093.en_US
dc.identifier.citedreferenceYamashita, K., Ollinger, R., McDaid, J., Sakahama, H., Wang, H., Tyagi, S., Csizmadia, E., Smith, N.R., Soares, M.P. & Bach, F.H. ( 2006 ) Heme oxygenase‐1 is essential for and promotes tolerance to transplanted organs. FASEB Journal, 20, 776 – 778.en_US
dc.identifier.citedreferenceZorca, S., Freeman, L., Hildesheim, M., Allen, D., Remaley, A.T., Taylor, J.G.t. & Kato, G.J. ( 2010 ) Lipid levels in sickle‐cell disease associated with haemolytic severity, vascular dysfunction and pulmonary hypertension. British Journal of Haematology, 149, 436 – 445.en_US
dc.identifier.citedreferenceAdams, R.J., McKie, V.C., Carl, E.M., Nichols, F.T., Perry, R., Brock, K., McKie, K., Figueroa, R., Litaker, M., Weiner, S. & Brambilla, D. ( 1997 ) Long‐term stroke risk in children with sickle cell disease screened with transcranial Doppler. Annals of Neurology, 42, 699 – 704.en_US
dc.identifier.citedreferenceAnthi, A., Machado, R.F., Jison, M.L., Taveira‐Dasilva, A.M., Rubin, L.J., Hunter, L., Hunter, C.J., Coles, W., Nichols, J., Avila, N.A., Sachdev, V., Chen, C.C. & Gladwin, M.T. ( 2007 ) Hemodynamic and functional assessment of patients with sickle cell disease and pulmonary hypertension. American Journal of Respiratory and Critical Care Medicine, 175, 1272 – 1279.en_US
dc.identifier.citedreferenceAtaga, K.I. & Orringer, E.P. ( 2003 ) Hypercoagulability in sickle cell disease: a curious paradox. American Journal of Medicine, 115, 721 – 728.en_US
dc.identifier.citedreferenceAtaga, K.I., Moore, C.G., Hillery, C.A., Jones, S., Whinna, H.C., Strayhorn, D., Sohier, C., Hinderliter, A., Parise, L.V. & Orringer, E.P. ( 2008 ) Coagulation activation and inflammation in sickle cell disease‐associated pulmonary hypertension. Haematologica, 93, 20 – 26.en_US
dc.identifier.citedreferenceBarrett, O. Jr, Saunders, D.E. Jr, McFarland, D.E. & Humphries, J.O. ( 1984 ) Myocardial infarction in sickle cell anemia. American Journal of Hematology, 16, 139 – 147.en_US
dc.identifier.citedreferenceBelcher, J.D., Mahaseth, H., Welch, T.E., Otterbein, L.E., Hebbel, R.P. & Vercellotti, G.M. ( 2006 ) Heme oxygenase‐1 is a modulator of inflammation and vaso‐occlusion in transgenic sickle mice. The Journal of Clinical Investigation, 116, 808 – 816.en_US
dc.identifier.citedreferenceBodary, P.F., Westrick, R.J., Wickenheiser, K.J., Shen, Y. & Eitzman, D.T. ( 2002 ) Effect of leptin on arterial thrombosis following vascular injury in mice. JAMA, 287, 1706 – 1709.en_US
dc.identifier.citedreferenceBoisvert, W.A., Spangenberg, J. & Curtiss, L.K. ( 1995 ) Treatment of severe hypercholesterolemia in apolipoprotein E‐deficient mice by bone marrow transplantation. The Journal of Clinical Investigation, 96, 1118 – 1124.en_US
dc.identifier.citedreferenceCampbell, A.D., Cui, S., Shi, L., Urbonya, R., Mathias, A., Bradley, K., Bonsu, K.O., Douglas, R.R., Halford, B., Schmidt, L., Harro, D., Giacherio, D., Tanimoto, K., Tanabe, O. & Engel, J.D. ( 2011 ) Forced TR2/TR4 expression in sickle cell disease mice confers enhanced fetal hemoglobin synthesis and alleviated disease phenotypes. Proceedings of the National Academy of Sciences of the United States of America, 108, 18808 – 18813.en_US
dc.identifier.citedreferenceDe Franceschi, L., Cappellini, M.D. & Olivieri, O. ( 2011 ) Thrombosis and sickle cell disease. Seminars in Thrombosis and Hemostasis, 37, 226 – 236.en_US
dc.identifier.citedreferenceDurante, W. ( 2010 ) Targeting heme oxygenase‐1 in vascular disease. Current Drug Targets, 11, 1504 – 1516.en_US
dc.identifier.citedreferenceEitzman, D.T., Westrick, R.J., Nabel, E.G. & Ginsburg, D. ( 2000 ) Plasminogen activator inhibitor‐1 and vitronectin promote vascular thrombosis in mice. Blood, 95, 577 – 580.en_US
dc.identifier.citedreferenceElsharawy, M.A., Moghazy, K.M. & Shawarby, M.A. ( 2009 ) Atherosclerosis in sickle cell disease ‐ a review. International Journal of Angiology, 18, 62 – 66.en_US
dc.identifier.citedreferenceFei, D., Meng, X., Zhao, M., Kang, K., Tan, G., Pan, S., Luo, Y., Liu, W., Nan, C., Jiang, H., Krissansen, G.W. & Sun, X. ( 2012 ) Enhanced induction of heme oxygenase‐1 suppresses thrombus formation and affects the protein C system in sepsis. Translation Research, 159, 99 – 109.en_US
dc.identifier.citedreferenceGerry, J.L., Bulkley, B.H. & Hutchins, G.M. ( 1978 ) Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. American Journal of Cardiology, 42, 211 – 216.en_US
dc.identifier.citedreferenceHanson, M.S., Piknova, B., Keszler, A., Diers, A.R., Wang, X., Gladwin, M.T., Hillery, C.A. & Hogg, N. ( 2011 ) Methaemalbumin formation in sickle cell disease: effect on oxidative protein modification and HO‐1 induction. British Journal of Haematology, 154, 502 – 511.en_US
dc.identifier.citedreferenceHoppe, C., Kuypers, F., Larkin, S., Hagar, W., Vichinsky, E. & Styles, L. ( 2011 ) A pilot study of the short‐term use of simvastatin in sickle cell disease: effects on markers of vascular dysfunction. British Journal of Haematology, 153, 655 – 663.en_US
dc.identifier.citedreferenceInoue, T., Plieth, D., Venkov, C.D., Xu, C. & Neilson, E.G. ( 2005 ) Antibodies against macrophages that overlap in specificity with fibroblasts. Kidney International, 67, 2488 – 2493.en_US
dc.identifier.citedreferenceIshikawa, K., Sugawara, D., Wang, X., Suzuki, K., Itabe, H., Maruyama, Y. & Lusis, A.J. ( 2001 ) Heme oxygenase‐1 inhibits atherosclerotic lesion formation in ldl‐receptor knockout mice. Circulation Research, 88, 506 – 512.en_US
dc.identifier.citedreferenceJadhav, A. & Ndisang, J.F. ( 2009 ) Heme arginate suppresses cardiac lesions and hypertrophy in deoxycorticosterone acetate‐salt hypertension. Experimental Biology and Medicine (Maywood), 234, 764 – 778.en_US
dc.identifier.citedreferenceJison, M.L., Munson, P.J., Barb, J.J., Suffredini, A.F., Talwar, S., Logun, C., Raghavachari, N., Beigel, J.H., Shelhamer, J.H., Danner, R.L. & Gladwin, M.T. ( 2004 ) Blood mononuclear cell gene expression profiles characterize the oxidant, hemolytic, and inflammatory stress of sickle cell disease. Blood, 104, 270 – 280.en_US
dc.identifier.citedreferenceJohns, D.G., Zelent, D., Ao, Z., Bradley, B.T., Cooke, A., Contino, L., Hu, E., Douglas, S.A. & Jaye, M.C. ( 2009 ) Heme‐oxygenase induction inhibits arteriolar thrombosis in vivo: effect of the non‐substrate inducer cobalt protoporphyrin. European Journal of Pharmacology, 606, 109 – 114.en_US
dc.identifier.citedreferenceJuan, S.H., Lee, T.S., Tseng, K.W., Liou, J.Y., Shyue, S.K., Wu, K.K. & Chau, L.Y. ( 2001 ) Adenovirus‐mediated heme oxygenase‐1 gene transfer inhibits the development of atherosclerosis in apolipoprotein E‐deficient mice. Circulation, 104, 1519 – 1525.en_US
dc.identifier.citedreferenceKato, G.J. & Gladwin, M.T. ( 2008 ) Evolution of novel small‐molecule therapeutics targeting sickle cell vasculopathy. JAMA, 300, 2638 – 2646.en_US
dc.identifier.citedreferenceKato, G.J., Gladwin, M.T. & Steinberg, M.H. ( 2007 ) Deconstructing sickle cell disease: reappraisal of the role of hemolysis in the development of clinical subphenotypes. Blood Reviews, 21, 37 – 47.en_US
dc.identifier.citedreferenceKim, H.J., Tsoy, I., Park, M.K., Lee, Y.S., Lee, J.H., Seo, H.G. & Chang, K.C. ( 2006 ) Iron released by sodium nitroprusside contributes to heme oxygenase‐1 induction via the cAMP‐protein kinase A‐mitogen‐activated protein kinase pathway in RAW 264.7 cells. Molecular Pharmacology, 69, 1633 – 1640.en_US
dc.identifier.citedreferenceLabbe, R.F., Vreman, H.J. & Stevenson, D.K. ( 1999 ) Zinc protoporphyrin: a metabolite with a mission. Clinical Chemistry, 45, 2060 – 2072.en_US
dc.identifier.citedreferenceLi, T., Tian, H., Zhao, Y., An, F., Zhang, L., Zhang, J., Peng, J., Zhang, Y. & Guo, Y. ( 2011 ) Heme oxygenase‐1 inhibits progression and destabilization of vulnerable plaques in a rabbit model of atherosclerosis. European Journal of Pharmacology, 672, 143 – 152.en_US
dc.identifier.citedreferenceLindenblatt, N., Bordel, R., Schareck, W., Menger, M.D. & Vollmar, B. ( 2004 ) Vascular heme oxygenase‐1 induction suppresses microvascular thrombus formation in vivo. Arteriosclerosis, Thrombosis, and Vascular Biology, 24, 601 – 606.en_US
dc.identifier.citedreferenceLinton, M.F., Atkinson, J.B. & Fazio, S. ( 1995 ) Prevention of atherosclerosis in apolipoprotein E‐deficient mice by bone marrow transplantation. Science, 267, 1034 – 1037.en_US
dc.identifier.citedreferenceLiu, X.M., Chapman, G.B., Wang, H. & Durante, W. ( 2002 ) Adenovirus‐mediated heme oxygenase‐1 gene expression stimulates apoptosis in vascular smooth muscle cells. Circulation, 105, 79 – 84.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Name:
bjh12342.pdf
Size:
407.3KB
Format:
PDF
View/Open

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.