June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
Tyrosinase reduces expression of vascular endothelial growth factors and improves corneal graft survival
Author Affiliations & Notes
  • Thomas Clahsen
    Department of Ophthalmology, Uniklinik Koln, Koln, Nordrhein-Westfalen, Germany
    University of Cologne Center for Molecular Medicine Cologne, Cologne, Nordrhein-Westfalen, Germany
  • Niloofar Hatami
    Department of Ophthalmology, Uniklinik Koln, Koln, Nordrhein-Westfalen, Germany
  • Christian Büttner
    Institute of Human Genetics, University Hospital Erlangen, Erlangen, Germany
  • André Reis
    Institute of Human Genetics, University Hospital Erlangen, Erlangen, Germany
  • Claus Cursiefen
    Department of Ophthalmology, Uniklinik Koln, Koln, Nordrhein-Westfalen, Germany
    University of Cologne Center for Molecular Medicine Cologne, Cologne, Nordrhein-Westfalen, Germany
  • Footnotes
    Commercial Relationships   Thomas Clahsen None; Niloofar Hatami None; Christian Büttner None; André Reis None; Claus Cursiefen None
  • Footnotes
    Support  DFG Cl751/1-1, Cl751/2-1
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 909 – A0273. doi:
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    • Get Citation

      Thomas Clahsen, Niloofar Hatami, Christian Büttner, André Reis, Claus Cursiefen; Tyrosinase reduces expression of vascular endothelial growth factors and improves corneal graft survival. Invest. Ophthalmol. Vis. Sci. 2022;63(7):909 – A0273.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Lymphangiogenesis is critically involved in immune responses and corneal graft rejection. Recently tyrosinase has been identified as a novel regulator of developmental and inflammation-induced lymphangiogenesis. However, the underlying mechanisms are still unknown. Here we analyze the influence of tyrosinase on proliferation and expression of vascular growth factors in vitro and in vivo and test whether tyrosinase influences graft survival.

Methods : Proliferation of human dermal lymphatic endothelial cells (HDLEC) with/without tyrosinase was measured by using IncuCyte Zoom. Expression of vascular endothelial growth factors was quantified in HDLECs in vitro and in central cornea in vivo by using qRT-PCR. Balb/c mice were subjected to corneal transplantations and received a 1.5 mm graft from C57B/6 mice or albino C57BL/6 (B6N-TyrcBrd) mice. Graft survival was determined over 8 weeks and immune cell frequencies in draining lymph nodes were analyzed 3 days and 8 weeks post-transplantation.

Results : Treatment of HDLECs with recombinant tyrosinase inhibited proliferation in a dose-dependent manner. The treatment of HDLECs with recombinant Tyrosinase resulted in a significantly reduced mRNA expression of VEGF-D, VEGF-R2, and -R3 in vitro.
In order to further analyze the influence of tyrosinase on lymphangiogenesis in vivo, the limbal lymph vessel architecture of naive C57BL/6 and B6N-TyrcBrd mice was compared. B6N-TyrcBrd mice showed a significant increase in lymph vessel area and a significantly higher number of endpoints and branch points. The quantitative RT-PCR of isolated central corneal RNA showed a significantly higher expression of VEGF-A, -C, VEGF-R2, and -R3 in B6N-TyrcBrd mice compared to C57BL/6 animals. BALB/c mice receiving grafts from B6N-TyrcBrd mice showed significantly reduced graft survival compared to animals grafted from C57BL/6 mice. No significant differences in the infiltration of immune cells into draining lymph nodes could be observed between the two groups.

Conclusions : In this study, we identify tyrosinase as a novel regulator for the expression of vascular endothelial growth factors in vitro and in vivo. Furthermore, tyrosinase seems to be a key player in regulating limbal lymphatic vessel architecture and corneal graft survival. A potential mechanism of how tyrosinase is involved in corneal graft rejection is this novel lymphangiogenesis modulating activity.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

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