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Complement factor involvement during experimental AMD
Linnæus Center of Biomaterials Chemistry, Linnæus University, Kalmar, Sweden.
Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
Linnæus Center of Biomaterials Chemistry, Linnæus University, Kalmar, Sweden; Department of Immunology, Genetics and Pathology, Uppsala University, Sweden.
2015 (English)In: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 67, no 1, 163-163 p.Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

Background and aim: Age-related macular degeneration (AMD) is the leading cause of severe vision loss in people over 60, occurring when the central part of the retina (macula) deterio-rates. Treatments of the neovascular form of AMD have progressed but not for the atrophic dry form, which is characterized by retinal pigment epithelial (RPE) cell dysfunction, retinal detachment and photoreceptor degeneration. The complement system has been acknowledged as a part of AMD-pathogenesis and suggested as a possible regulator of AMD progression. Different complement factors, both activating and inactivating elements, have been found in drusen; the clinical hallmark of AMD. The mechanism and underlying association of the complement system in AMD is incomplete and further investigations are needed. RPE cell and retinal tissue interactions, complement factor secretion and gene expressions were investigated.

Methods: Post-confluent human RPE-cells were cultured with or without adult porcine retinas for three and five days in vitro. RPE-cell and retinal explant interactions were morphologically investigated by immunohistochemistry and lectin staining. The release of complement factors (C1q, C3, factor H, factor I and C4BP) was investigated by using Luminex xMAP technology and gene expression was investigated by real-time PCR, respectively.

Results: Post-confluent RPE cells expressed zonula occludens-1 (ZO-1) immunoreactivity suggesting the presence of tight junctions in the cytoplasmic membrane. RPE-cells and retinal tissue showed preserved morphology and normal layering after co-culture. C1q, C3, factor H and factor I was secreted into the supernatants after the culturing process and RPE-cells were shown to express C1q, factor H and factor I.

Conclusions: RPE-cell and retinal tissue integrity is preserved in the co-cultures. Complement system proteins appear to be locally produced and possibly a part of the pathogenesis during experimental AMD.

Place, publisher, year, edition, pages
2015. Vol. 67, no 1, 163-163 p.
National Category
Immunology in the medical area
Research subject
Immunology
Identifiers
URN: urn:nbn:se:oru:diva-45531ISI: 000357144100140OAI: oai:DiVA.org:oru-45531DiVA: diva2:845779
Conference
15th European Meeting on Complement in Human Disease (EMCHD), Uppsala, Sweden, June 27-30, 2015
Available from: 2015-08-13 Created: 2015-08-12 Last updated: 2017-10-17Bibliographically approved

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