gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

Alkylphosphocholines inhibit attachment, spreading and migration of human retinal pigment epithelial cells

Meeting Abstract

  • corresponding author D. Kook - Department of Ophthalmology, University Eye Hospital, LMU Munich, Munich
  • U. Welge-Lüßen - Department of Ophthalmology, University Eye Hospital, LMU Munich, Munich
  • S. Priglinger - Department of Ophthalmology, University Eye Hospital, LMU Munich, Munich
  • A. Ohlmann - Department of Ophthalmology, University Eye Hospital, LMU Munich, Munich
  • A. Kampik - Department of Ophthalmology, University Eye Hospital, LMU Munich, Munich
  • K.H. Eibl - Department of Ophthalmology, University Eye Hospital, LMU Munich, Munich

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogP 176

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dog2004/04dog667.shtml

Veröffentlicht: 22. September 2004

© 2004 Kook et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective

Proliferative Vitreoretinopathy (PVR) is a major cause for visual loss after retinal detachment surgery. The dispersion of retinal pigment epithelial cells (RPE) in the vitreous seems to be fundamental in PVR membrane formation and subsequent retinal detachment. The aim of our study was to test if Alkylphosphocholines (APCs) are able to prevent early cellular events in PVR development like attachment, spreading und migration of human RPE cells in vitro.

Methods

Cultured RPE cells of five human donors were treated with one of four APCs (C18:1-PC, C20:1-PC, C21:1-PC or C22:1-PC) in different concentrations in DMEM/10% FCS. Cell viability was tested by the trypan blue exclusion assay. Attachment was assessed after a 2 h incubation of RPE cells on coated 24-well-plates and subsequent MTT testing. Cellular spreading is characterized by cytoplasmic halo formation and was quantified by counting four separate fields of RPE cells allowed to spread on coated 24-well-plates for 4 h. Migration was assessed by a modification of the Boyden chamber method in microchemotaxis chambers with polycarbonated filters.

Results

All four APCs could inhibit RPE cell attachment and spreading by > 70% at their IC50 concentration (C18:1-PC: 30mM; C20:1-PC: 10mM; C21:1-PC: 10mM; C22:1-PC: 10mM). Also, APCs were able to inhibit RPE cell migration by > 95% at similar concentrations. Trypan blue staining revealed a toxicity within control limits in the concentration interval tested.

Conclusions

APCs are able to inhibit RPE cell attachment, spreading and migration in vitro at non-toxic concentrations. This could be a novel method to prevent even early stages of PVR development.