Macular Degeneration / iron

Discussion in 'Optometry Archives' started by babawali, May 8, 2006.

  1. babawali

    babawali Guest

    "the present study suggests that altered iron homeostasis is associated
    with AMD.

    What causes the change in homeostasis that causes iron to be increased in
    those with AMD, and therefore is the initial cause for it?
     
    babawali, May 8, 2006
    #1
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  2. babawali

    ironjustice Guest

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    (Investigative Ophthalmology and Visual Science. 2006;47:2135-2140.)
    © 2006 by The Association for Research in Vision and Ophthalmology,
    Inc.
    DOI: 10.1167/iovs.05-1135

    The Iron Carrier Transferrin Is Upregulated in Retinas from Patients
    with Age-Related Macular Degeneration
    Itay Chowers,1 Robert Wong,2 Tzvete Dentchev,2 Ronald H. Farkas,3 Jared
    Iacovelli,2 Tushara L. Gunatilaka,3 Nancy E. Medeiros,4 J. Brett
    Presley,5 Peter A. Campochiaro,3,6 Christine A. Curcio,5 Joshua L.
    Dunaief,2 and Donald J. Zack3,6,7,8
    1From the Department of Ophthalmology, Hadassah-Hebrew University
    Medical Center, Jerusalem, Israel; the 2F. M. Kirby Center for
    Molecular Ophthalmology, Scheie Eye Institute, Philadelphia,
    Pennsylvania; the 3Guerrieri Center for Genetic Engineering and
    Molecular Ophthalmology, Wilmer Ophthalmological Institute, Department
    of Ophthalmology, and 6Departments of Neuroscience and 7Molecular
    Biology and Genetics, and the 8McKusick-Nathans Institute of Genetic
    Medicine, The Johns Hopkins University School of Medicine, Baltimore,
    Maryland; 4Retina Specialists of North Alabama, Huntsville, Alabama;
    and the 5Department of Ophthalmology, University of Alabama,
    Birmingham, Alabama.


    PURPOSE. Iron can cause oxidative stress, and elevated iron levels have
    been associated with several neurodegenerative diseases including
    age-related macular degeneration (AMD). Transferrin, an iron transport
    protein, is expressed at high levels in the retina. The purpose of this
    study was to assess transferrin involvement in AMD by determining the
    expression profile of transferrin in retinas with AMD compared with
    retinas without evidence of disease.

    METHODS. Postmortem retinas were obtained from AMD and non-AMD eyes.
    Expression of transferrin was assessed in a microarray dataset from 33
    retinas of unaffected donors and 12 retinas of patients with AMD (six
    with neovascular AMD and six with non-neovascular AMD). Quantitative
    real-time RT-PCR (QPCR) was used to confirm the microarray results.
    Transferrin protein expression was assessed by semiquantitative Western
    blot analysis and immunohistochemistry.

    RESULTS. In comparison to unaffected retinas, mean transferrin mRNA
    levels, as measured by microarray analysis were elevated 3.5- and
    2.1-fold in non-neovascular and neovascular AMD retinas, respectively.
    Semiquantitative Western blot analysis demonstrated a 2.1-fold increase
    in transferrin protein in AMD eyes. Immunohistochemistry showed more
    intense and widespread transferrin label in AMD maculas, particularly
    in large drusen, Müller cells, and photoreceptors.

    CONCLUSIONS. These data demonstrate that transferrin expression is
    increased in the retinas of patients with AMD relative to those of
    healthy control patients of comparable age. Along with previous studies
    that have demonstrated elevated iron levels in AMD retinas, early onset
    drusen formation in a patient with retinal iron overload resulting from
    aceruloplasminemia, and retinal degeneration with some features of
    macular degeneration in the iron-overloaded retinas of
    ceruloplasmin/hephestin knockout mice, the present study suggests that
    altered iron homeostasis is associated with AMD.



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    ironjustice, May 9, 2006
    #2
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