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Differences between type 1 and type 2 diabetics in retinal neovascular tissue and vitreous humour
  1. Kati Kinnunen (kati.kinnunen{at}uku.fi),
  2. Tuomo Puustjärvi (tuomo.puustjarvi{at}kuh.fi),
  3. Markku Teräsvirta (markku.terasvirta{at}kuh.fi),
  4. Piia Nurmenniemi (piia.nurmenniemi{at}epshp.fi),
  5. Tommi Heikura (tommi.heikura{at}uku.fi),
  6. Svetlana Laidinen (laidinen{at}hytti.uku.fi),
  7. Timo Paavonen (timo.paavonen{at}pshp.fi),
  8. Hannu Uusitalo (hannu.uusitalo{at}pshp.fi),
  9. Seppo Ylä-Herttuala (seppo.ylaherttuala{at}uku.fi)
  1. Kuopio University Hospital, Finland
  2. Kuopio University Hospital, Finland
  3. Kuopio University Hospital, Finland
  4. Kuopio University Hospital, Finland
  5. Kuopio University, Finland
  6. Kuopio University, Finland
  7. Tampere University, Finland
  8. Tampere University, Finland
  9. Kuopio University, Finland

    Abstract

    Aims: Evaluate the histopathology of neovascular tufts and vitreous samples collected from diabetic patients.

    Methods: Vitreous samples and neovascular tufts were collected from type 1 (n=13) and type 2 diabetics (n=17) with proliferative retinopathy and controls with macular hole (n=5). Neovessels were analyzed using immunohistochemistry and vitreous samples with Enzyme-linked immunosorbent assay (ELISA). Main outcome measure was to find differences in growth factors in proliferative retinopathy between type 1 and type 2 diabetics.

    Results: VEGF-A was most strongly present in the samples in type 1 diabetics. In type 2 diabetics, VEGF-D was more abundantly present than in type 1 diabetics. Also ANG-2 was abundantly present. Macrophages and nuclear factor kappa B (NFκB) were found indicating the presence of an inflammatory process in the neovascular tissues.

    Conclusions: VEGF-A and ANG-2 are equally important in neovascular process in both type 1 and type 2 diabetics. In type 2 diabetics, VEGF-D is abundantly present. To achieve better control of diabetic retinopathy, it might be beneficial to target also against the actions of ANG-2 and VEGF-D.

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